Database for Annotation, Visualization and Integrated Discovery 2.1
National Institute of Allergy and Infectious Disease
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snail family transcriptional repressor 1(SNAI1) snail family transcriptional repressor 1(SNAI1) Related Genes Homo sapiens
CYTOBAND 20q13.1-q13.2,
GENERIF_SUMMARY Snail expression inversely correlates with the grade of differentiation of the tumours and that it is expressed in all the infiltrating ductal carcinomas (IDC) presenting lymph node metastases that were analysed., SNA1 plays a role in repressing E-cadherin and MUC1 in epithelial cells, Snail is a new inducer of MMP-2 expression which contributes to the increased invasion of squamous cell carcinoma cells, E-cadherin and claudins/occludin have roles in the regulation of tight junctions during the epithelium-mesenchyme transition, but are repressed by snail, Hypoxia induces down-regulation of E-cadherin in ovarian carcinoma cells, via up-regulation of the transcriptional repressor SNAIL., Snail expression may be induced during hepatocellular cell carcinoma progression; Snail directly represses gene transcription and activates invasion via upregulation of MMP gene family, Results indicate that Snail is involved in both the direct transcriptional repression of genes and post-transcriptional.These data support the idea that Snail is a transcription factor possessing pleiotropic activities., Snail transcription is driven by signaling pathways known to induce epithelial to mesenchymal transition, reinforcing the role of Snail in this proces, Results suggest that aberrant expression of Snail or Slug may promote tumorigenesis through increased resistance to programmed cell death., SNAl1 is regulated by GSK-3beta-mediated phosphorylation in control of epithelial-mesenchymal transition., E-cadherin mRNA expression in synovial sarcoma was associated with reduced Snail expression level, Data show that the activity of glycogen synthase kinase-3 (GSK-3) is necessary for the maintenance of the epithelial architecture, and that GSK-3 inhibition stimulates the transcription of Snail., Wnt signaling stabilizes Snail and beta-catenin proteins in tandem fashion so as to cooperatively engage transcriptional programs that control an epithelial-mesenchymal transition., demonstrated, for the first time, that SNAIL is upregulated in colon cancer, which potentially may have significance in control of metastasis and possibly serve as a target for chemopreventive agents, Over expression of Smad-interacting protein 1 is associated with ovarian carcinoma aggressiveness, zinc finger domain functions as a nuclear localization signal, can be transported into the nucleus by importin beta-mediated, Snail may play a role in recurrence by downregulating E-cadherin and inducing an epithelial-to-mesenchymal transition in breast cancer., SNAIL expression in colorectal tumors is associated with downregulation of E-cadherin (CDH1) and vitamin D receptor gene products, Human cancers that overexpress snail may have a survival advantage to genotoxic and potentially other forms of stress, The pattern of Snail expression suggests only a minor role of Snail in tumours of the upper gastrointestinal tract., Snail is present in activated mesenchymal cells indicating its relevance in the communication between tumor and stroma and suggest that it can promote the conversion of carcinoma cells to stromal cells., These findings indicate that Snail upregulation by HGF is mediated via the MAPK/Egr-1 signaling pathway and that both Snail and Egr-1 play a critical role in HGF-induced cell scattering, migration, and invasion., These results indicate that NBS1 overexpression induces EMT through the upregulation of Snail expression, and co-expression of NBS1/Snail predicts metastasis in HNSCCs, VHL promotes E2 box-dependent E-cadherin transcription by HIF-mediated regulation of SIP1 and snail, The identification of a beta-catenin-T-cell factor-regulated Axin2-GSK3beta-Snail1 axis provides new mechanistic insights into cancer-associated epithelial-mesenchymal transition programmes., Overexpression of a constitutively activated IGF-IR (CD8-IGF-IR) was sufficient to cause transformation of immortalized human mammary epithelial cells and growth in immunocompromised mice., Snail regulates the activity of PRL-3 gene by binding to the promoter of PRL-3 gene in SW480 cells., the Snail promoter is constitutively packaged in a poised chromatin structure that can be activated in melanoma cells by a tissue-specific enhancer, which physically contacts the promoter, Snail1 is involved in renal tubular EMT and TGF-beta1 regulates Snail1 at the transcription and protein degradation levels, Data show that SNAI1 and SNAI2 are ectopically expressed in thyroid carcinomas, and aberrant expression in mice is associated with papillary carcinoma development., Snail and SHH are overexpressed in a large subset of NETs of the ileum., RKIP is a novel component of the Snail transcriptional regulatory network important for the progression and metastasis of cancer., Snail is associated with lower overall survival of ovarian cancer patients., These data are in line with a proposed role for Snail in endometrial tumor progression., Analysis of cell lines derived from lymph node metastasis indicates that SNAI1 expression is required for metastatic dissemination., These data show that Snail functions as a molecular mediator of TGF-beta1-regulated MMP-9 expression by increasing Ets-1 and thereby contributing to oral cancer progression., These results lead to a new hypothesis that Snail and ZEB1 are downstream of CCN6 and play a critical role in CCN6-mediated regulation of E-cadherin in breast cancer., A positive feedback stimulation of the Wnt pathway by activation of snail., A novel autocrine function for VEGF in breast tumor cells in driving the expression of Snail, a breast tumor progression factor., Overexpression of Snail is associated with up-regulation of proinflammatory mediators and inhibits differentiation in oral keratinocytes and thus head and neck squamous cell carcinomas, EGF cooperates with alpha(5)beta(1) integrin signaling to induce EMT in cervical cancer cells via up-regulated Snail, These results suggest that bile acids repress E-cadherin through the induction of transcription factor Snail, Snail and Slug promote formation of beta-catenin-T-cell factor (TCF)-4 transcription complexes that bind to the promoter of the TGF-beta3 gene to increase its transcription., HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression., class I histone deacetylase (HDACs), specifically HDAC2, and the transcriptional repressor Snail play a central role in the suppression of 15-hydroxyprostaglandin dehydrogenase expression., Factors released by breast cancer cells are able to upregulate Snail expression in vascular endothelial cells., The Snail-p53 binding as the new therapeutic target for K-Ras-mutated cancers including pancreatic, lung, and colon cancers., Snail1-mediated suppression of CYLD plays a key role in melanoma malignancy., Snail expression in oral squamous cell carcinoma is a stromal phenomenon associated with the myofibroblast phenotype and not related to growth-factor-mediated transdifferentiation of the carcinoma cells themselves., Snail1 expression was significantly increased in PC with a positive correlation to dedifferentiation, but not to cancer progression or prognosis., Snail upregulation by HRG-beta1 is mediated via the PI3K/Akt signaling pathway and Snail plays a key role in HRG-beta1 induced breast cancer cell metastasis through induction of EMT, Study provides evidence that p53, binding with Snail, is exported from a K-Ras-mutated cell through a vesicle transport-like mechanism, independently using a p53-nuclear-exporting mechanism., We found upregulation of mRNA for transcription factors Snail, Slug, Twist, and SIP1 in spindle cell carcinoma when compared to squamous cell carcinoma., Data show that several importins mediate the nuclear import of human Snail1 and identify a unique nuclear localization signal, recognized by all the importins, that has been conserved during the evolution of the Snail family., We describe for the first time that EMT markers Snail and Twist are expressed in PCC and that their expression is associated with malignancy, The results indicate that the presence of nuclear Snail1 immunoreactive cells in the stroma may be an informative indicator of prognosis of colon tumours especially useful in those corresponding to lower stages., study suggests the possibility that circulating Snail mRNA levels may have been associated with extra-hepatic metastasis in hepatocellular carcinoma patients, EGFR signalling is involved in Snail protein overexpression, EGF-mediated EMT is augmented by staurosporine in PMC42-LA cells through actin depolymerisation, focal contact size reduction and Snail1 induction, High frequency of SNAIL-expressing cells is associated with metastatic potential of phaeochromocytoma., Ladybird homeobox 1 (LBX1), a developmentally regulated homeobox gene, directs expression of the known EMT inducers ZEB1, ZEB2, Snail1, and transforming growth factor beta2 (TGFB2)., Nuclear expression of Snail1 protein in epithelial ovarian tumours was increased during tumour progression from precursor lesions into carcinomas., Data show that elevated Snail expression by Pdcd4 knockdown leads to downregulation of E-cadherin resulting in activating beta-catenin/Tcf-dependent transcription., The role of Snail in the inflammation-induced promotion of epithelial-mesenchymal transition in head and neck squamous cell carcinoma., Snail plays a critical role in tumor growth and metastasis of ovarian carcinoma through regulation of MMP activity., Histologically normal tissue adjacent to tumor tissue expressing the epithelial-mesenchymal transition-inducing gene SNAI1 shows alterations in the expression of epithelial differentiation genes such as CDH1 and VDR., Coexpression of Snail and Twist correlated with the worst prognosis of hepatocellular carcinoma., Alcohol stimulated nuclear localization of Snai1 phosphorylated at Ser246, and transcription from a Snai1 reporter plasmid and Snai1 mRNA expression., The present study demonstrated that Snai1 plays a role in colorectal cancer (CRC) invasion through phosphorylation, suggesting a plausible mechanism for overcoming chemoresistance that will lead to the development of effective treatments for CRC., Snail upregulation plays a role in non-small cell lung carcinoma by promoting tumor progression mediated by CXCR2 ligands, Induction of a MT1-MMP and MT2-MMP-dependent basement membrane transmigration program in cancer cells by Snail1., These results highlight serines 11 and 92 as new players in Snail1 regulation and suggest the participation of CK2 and PKA in the modulation of Snail1 functionality., study demonstrates that the F-box E3 ubiquitin ligase FBXl14 interacts with SNAIL1 and promotes its ubiquitylation and proteasome degradation independently of phosphorylation by GSK-3beta, nuclear expression parallels higher malignancy in neuroendocrine lung tumors, Snail expression (n = 22) correlated with ILK expression in ductal pancreatic adenocarcinoma (rho = 0.8168, p = 0.02), but only minimal Snail staining activity was detected in PanIN lesions., transcription factors Snail1 and Snail2 repress vitamin D receptor during colon cancer progression, p63 isoforms are regulated by snail and slug transcription factors in human squamous cell carcinoma, Snail transcription factor regulates neuroendocrine differentiation in LNCaP prostate cancer cells, These results suggest a direct role for Notch signalling via the Snail pathway in the development of epithelial to mesenchymal transformation and renal fibrosis., Snail acts primarily as a survival factor and inhibitor of cellular senescence in prostate cancer cell lines. Snail can act as early driver of prostate cancer progression., Low expression of E-CD and high expression of Snail are related to the advanced stage, and poor prognosis in colorectal cancer patients., identified a set of novel Snail1 target proteins in colon cancer that expand the cellular processes affected by Snail1 and thus its relevance for cell function and phenotype, These results suggest that epithelial-mesenchymal transition induced by TGF-beta1/Snail activation is closely associated with the aggressive growth of cholangiocarcinoma, resulting in a poor prognosis., Hypoxia-inducible factor-1alpha induces down-regulation of CDX2 in colon carcinoma cells and Snail may be involved in this regulation process., A nonpredicted link between SNAI1-triggered EMT and the down-regulation of Nectin-1 and StarD10 through the up-regulation of miR-661, which may contribute to the invasion of breast cancer cells and poor disease outcome., Snai1 physically interacts with and recruits the histone demethylase LSD1 (KDM1A) to epithelial gene promoters., These results indicate that SNAIL-mediated EMT may be relevant in the progression of pancreatic cancer, differentially regulated by hypoxia and hyperglycemia in kidney proximal tubule cells, Activation of ERCC1 by Snail is critical in the generation of cisplatin resistance of head and neck squamous cell carcinoma cells., The present study showed that Snail induces several Epithelial-mesenchymal transition related genes in primary cultured human keratinocytes., Snail-induced EMT represents a clinically relevant mechanism of upper urinary tract urothelial carcinoma (UTUC) progression and an attractive target for the treatment of patients with UTUC., Snail1 may play important role in invasion and metastasis of ACC; Snail1 has potential for being a strong prognosis indicator at presentation of ACC patients., Interaction of Snail and p38 mitogen-activated protein kinase results in shorter overall survival of ovarian cancer patients., Hyperglycaemic condition enhances O-GlcNAc modification and initiates epithelial-mesenchymal transition by transcriptional suppression of E-cadherin through Snail1., Role for Snail1 transcription factor in hepatic wound-healing response and its involvement in hepatic stellate cell transdifferentiation process., Results suggested that SNAI1 is involved in the proliferation and migration of glioblastoma cells., Transciption factor SNAIL1 mimics the histone H3 tail and binds to the histone demethylase LSD1-transcription co-repressor (CoREST) complex. The crystal structure of the complex is given here., Collectively, our studies demonstrate frequent expression of nuclear Snail1, but not nuclear ZEB1, in invasive, triple-negative breast cancers as well as in intraductal carcinomas., Snail, a major player in the process of epithelial-to-mesenchymal transition, is highly expressed by tubular epithelial cells during multiple myeloma nephropathy., The results indicate that Snail1 controls Zeb1 expression at multiple levels and acts cooperatively with Twist in the ZEB1 gene transcription induction., In BPH-1 cells the transcription factor SNAI2/Slug is important for epithelial-mesenchymal transition initiation, Expression of snai1, or expression of zeb1 or twist in the stromal compartment did not have any prognostic significance., The presence of snail1 protein in tumour microenvironment rather than in malignant epithelial tumour cells may induce tissue remodelling and tumour progression., Snail is implicated in metabolic stress-induced necrosis, providing a new function for Snail in tumor progression., regulatory mechanism of the nuclear protein import process by importin alpha may control Snail activity by inhibiting its nuclear localization, Snail1 activity results in increased MMPs and decreased E-Cadherin expression., A novel regulatory mechanism was characterized which controls Snail1 protein expression through poly(ADP-ribosyl)ation. The effect was not only limited to repression of Snail1 transcription but also to downregulated Snail1 protein stability., findings indicate that Snail is an important modulator of therapeutic responses of pancreatic cancer cells and is potentially useful as a sensitizer in pancreatic cancer therapy., Snail is a major transcriptional factor for epithelial-mesenchymal transition (EMT) in choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD)., These results suggest that miR-30a targets Snai1, inhibits invasion and metastasis, and is downregulated in NSCLC, No significant variability in Snail expression levels in the primary breast tumors nor in their metastases was found., Snail and Zeb1 were sufficient to induce epithelial to mesenchymal transition (EMT) in the cells, but activated TGFbeta induced a more complex EMT, in which changes in extracellular matrix remodeling components were pronounced., Sna1 directly induced transcription of N-Myc in human medulloblastoma cells. Depletion of N-Myc ablated the Sna1-induced proliferation and transformation., Data suggest a critical role of EZH2 in the control of cell invasionand/or metastasis by forming a co-repressor complex with HDAC1/HDAC2/Snail to repress E-cadherin., SNAIL and TWIST play a crucial role in epithelial to mesenchymal transition through regulation of E- and N-cadherin expression, exclusively in estrogen receptor-positive breast cancer patients., Snail has important role in invasion and metastasis, and silencing gene may be potential therapeutic target in renal cell carcinoma., Overexpression of Snail, Slug, and dysadherin and activation of Wnt and PI3K/Akt signaling was associated with inactivated E-cadherin in the spindle cells of monophasic fibrous synovial sarcomas., High SNAIL1 is associated with Crohn's disease-associated fistulae., TWIST and SNAI1 expression in stromal cells is associated with clinical and histopathological characteristics that indicate progressive disease. Negative expression of these EMT-promoting transcription factors predicts a better outcome., Authors observed up regulation of TGF-beta, Twist, Snail, Slug, vimentin and down regulation of E-cadherin on infection of ovarian tumor cells with Ad-PTTG cDNA., Snail transcription factor plays a critical role in TGF-beta1-induced epithelial-mesenchymal transition in human retinal pigment epithelium cells., novel evidence that inhibition of BMP-2 or BMP-2-mediated MAPK/Runx2/Snail signaling is an attractive therapeutic target for osteolytic bone metastases in lung cancer patients., Lats2 interacts with Snail1 and directly phosphorylates Snail1 at residue T203., Snail-1/VDR/beta-catenin signaling reflects an important underlying mechanism of osteosarcoma progression, in both nontumorigenic and tumorigenic epithelial cancer cells, that Snail1 is uniquely required for EMT initiation, whereas Twist1 is required to maintain late EMT, the EMT and invasion programs initiated by p53 loss of function or mutation are completely dependent on Snail1 expression, a global view of the impact of Snail and Slug expression, NOTCH1 intracellular domain interaction with Snail was found to induce ubiquitination and MDM2-dependent degradation of SNAIL., miR-9 inhibits melanoma proliferation and metastasis through down-regulation of the NF-kappaB1-Snail1 pathway., miR-34 and SNAIL form a double-negative feedback loop to regulate epithelial-mesenchymal transitions., Snail1 enhances the binding of Akt2 to the E-cadherin (CDH1) promoter and Akt2 interference prevents Snail1 repression of CDH1 gene, PGE(2)/EP4/p-Akt has a role in Snail signaling and conferring cell survival advantage, High co-expression of vascular endothelial growth factor receptor-1 and Snail is associated with poor prognosis after curative resection of hepatocellular carcinoma., investigated the direct role of YY1 in the regulation of EMT. This review discusses the molecular regulation of EMT in cancer cells through the activity of the dysregulated NF-kappaB/Snail/ YY1/PTEN/RKIP circuitry, Findings indicate that galiximab inhibits the NF-kappaB/Snail/YY1/Bcl-XL circuit that regulates drug resistance in B-cell lymphoma and in combination with cytotoxic drugs results in apoptosis., Data showed that regulation of SNAI1 through PKD1 occurs in vivo in normal breast ductal tissue and is decreased or lost in invasive ductal carcinoma., the results obtained demonstrate the phenomenon of Snail1 activation in the hormone-resistant breast cancer cells, SNAI1 expression induces an increase in the number of CD133+ cells, a change important for the epithelial to mesenchymal transition and the proliferation in ovarian cancer., Overexpression of Snail induces epithelial to mesenchymal transition and promotes cancer stem cell -like traits in the SCC9 cells., These findings suggest that Smad3 and Snail have circadian rhythm in vitro and vivo, and that circadian expression of Smad3 depends on CLOCK/BMAL1., Reelin is an essential negative regulator in the TGF-beta1-induced cell migration process, and is suppressed by TGF-beta pathway at the transcriptional level through Snail regulation, Snail interacted with G9a, a major euchromatin methyltransferase responsible for H3K9me2, and recruited G9a and DNA methyltransferases to the E-cadherin promoter for DNA methylation., dystopic subcellular localizations of Snail-1 and claudin-1 may participate in changes of cellular morphology and behavior which might be associated with altered effectory pathways of proteins and thus substantially contribute to the cancer development., High snail is associated with invasion and metastasis of gastric cancer., Data suggest that Snail expression could be a reliable independent prognostic factor to predict gastric carcinoma progression, which might open a new avenue for potential clinical intervention with functional Snail expression in gastric cancer patients., Data propose a novel EMT core network integrating two fundamental negative feedback loops, miR203/SNAI1 and miR200/ZEB., Snail interacted with Suv39H1 and recruited it to the E-cadherin promoter for transcriptional repression., Unbalanced expression of CK2 kinase subunits is sufficient to drive epithelial-to-mesenchymal transition by Snail1 induction., High snail1 is associated with migration and invasion of tongue squamous cell carcinoma., Hugl-2 induces MET and suppresses Snail tumorigenesis., hyperglycemia caused an induction of phosphorylated extracellular signal-related kinase 1/2 and Snail1 that was abrogated by silencing of TrkA or CCN2 using small interfering RNA, Decrease in the estrogen dependency of breast cancer cells is accompanied by an increase in Snail1 expression and activity, and demonstrated the Snail1 involvement in the negative regulation of ER., Axin2 acts as a potent promoter of carcinoma behavior by up-regulating the activity of the transcriptional repressor, Snail1, inducing a functional epithelial-mesenchymal transition (EMT) program and driving metastatic activity, Snail1 and its phosphorylation at Ser-11 were required and sufficient to control PKD1-mediated anchorage-independent growth and anchorage-dependent proliferation of different tumor cells, Invasiveness was significantly correlated to the increased Snail in tumour cells, as well as to increased ASMA, S100A4, and PDGFRbeta in stromal cells., changes in the expression of Snail or E-cadherin might regulate Epithelial-mesenchymal transition development in cholangiocarcinoma, the ATM-Snail pathway promotes tumor metastasis, highlighting a previously undescribed role of the DDR in tumor invasion and metastasis., Ectopic expression of Snail and Twist contributed to lymph node and disseminated metastasis, respectively, by reducing E-cadherin expression, providing a novel role for Snail and Twist in the progression of colorectal cancer., SNAI1 expression was significantly correlated with lower expression of CDH1 in colorectal adenoma., It might play an important role in the implantation of metastatic foci., these studies support the concept that targeting Snail/Slug-dependent transcription repression complexes by inhibiting LSD1 may lead to the development of novel drugs selectively inhibiting the invasive potential of cancer cells., Snail and Claudin-3 may play important roles in invasion and metastasis in NSCLC, Snail signaling contributes to prostate cancer progression and metastasis.[Review], transcription factor GLI1 mediates TGFbeta1 driven EMT in hepatocellular carcinoma via a SNAI1-dependent mechanism, Snail-dependent production of Cyr61 in epithelial mesenchymal transformation-phenotypic cells could prime and promote dynamic cell migration of the invasive tumor nest., High Snail1 expression is associated with nasopharyngeal neoplasms, Loss of E-cadherin may be mediated through NF-kappaB-induced Snail upregulation., Snail regulates levels of E-cadherin and desmoglein 2 in oral squamous cell carcinoma cells both transcriptionally and post-translationally., Snail down-regulates COX-2 in cutaneous squamous cell carcinoma cells., ALX1 upregulated expression of the key EMT regulator Snail (SNAI1) and that it mediated EMT activation and cell invasion by ALX1., Overexpression of snail induces epithelial-mesenchymal transition and a cancer stem cell-like phenotype in human colorectal cancer cells., AKT/GSK-3beta-mediated stabilization of Snail is required for TNFalpha-induced epithelial-mesenchymal transition in colorectal cancer cells, BRAF(V600E) increases migration and invasion of thyroid cancer cells via upregulation of Snail with a concomitant decrease of its target E-cadherin., Snail1 phosphorylation by DNA-PKcs was involved in genomic instability and aggressive tumor characteristics., Snail decreased transcription of Notch1 intracellular domain (NICD) target genes via competing with MAML1, co-activator, in NICD complex., Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1alpha in hepatocellular carcinoma., Down-regulation of MTA3 and up-regulation of CGB5 and Snail are associated with preeclampsia., Snail1 expression was detectable in most of the CRC but showed no significant association with E-cadherin loss, clinical pathological characteristics or overall survival., Snail, acting downstream of bone morphogenetic protein signaling, dissociates the invasive capacity of glioblastoma multiforme cells from their tumorigenic potential., Data indicate that Fas signalling inactivates GSK-3beta by ERK/MAPK signalling, leading to nuclear accumulation of Snail and beta-catenin., Data indicate that miR-106b-25 cluster (miR-106b, miR-93 and miR-25) targets the 3'UTR of the beta-TRCP2 transcript and increases the expression of Snail., DDR2 maintains SNAIL1 level and activity in tumour cells that have undergone epithelial-mesenchymal transition (EMT), thereby facilitating continued tumour cell invasion through collagen-I-rich extracellular matrices by sustaining the EMT phenotype., Data indicate that pancreatic (pro)enzymes enhanced expression of beta-catenin and E-cadherin and decreased expression of several epithelial-mesenchymal transition (EMT)-associated genes, such as Vimentin, Snail and Slug., Angiotensin II plays a role in glomerular injury in experimental and human diabetic nephropathy via persistent activation of Notch1 and Snail signaling in podocytes resulting in down-regulation of nephrin expression., Results suggest that Snail contributes to pancreatic tumor development by promoting fibrotic reaction through increased TGF-beta signaling., AIB1 exerted its effect on epithelial mesenchymal transition through its interaction with ERalpha, which could directly bind to the ERalpha-binding site on the SNAI1 promoter., High SNAIL expression is associated with hepatocellular carcinoma., Down-expression of Snail reversed GLI1 activation-regulated expression of epithelial--mesenchymal transition markers., The nuclear protein expression levels of SNAI1 and ZEB1 are involved in the progression and lymph node metastasis of cervical cancer via the epithelial-mesenchymal transition pathway., DYRK2 controls the epithelial-mesenchymal transition in breast cancer by degrading Snail., Snail1-mediated suppression of Cezanne2 may have a key role in HCC malignancy., EMT-induced stem/progenitor cell activation process is tightly regulated in non-transformed MCF10A cells, as WNT5A and TGFB2 are strongly upregulated in MCF10A-SNAI1 cells antagonizing canonical Wnt pathway, Loss of SNAI1 protein expression is associated with bladder cancer., miR-30a negatively regulates Snai1-mediated EMT during peritoneal fibrosis in vitro and in vivo., celastrol downregulates Snail expression, thereby inhibiting TGF-beta1-induced EMT in MDCK and A549 cells, VAV1 overexpression in both SKOV3 and human ovarian surface epithelial cells demonstrated that its upregulation of an E-cadherin transcriptional repressor, Snail and Slug, was not confined to ovarian cancer cells, ATM-mediated Snail Serine 100 phosphorylation in response to ionizing irradiation plays an important part in the regulation of radiosensitivity., Snail, a zinc-finger transcriptional repressor, was shown to be a mediator of NDRG2-regulated E-cadherin expression., The data show that Snail1 and beta-catenin, besides association with loss of hormone dependence, protect cancer cells from hypoxia and may serve as an important target in the treatment of breast cancer., HIF-1alpha and Snail are responsible for hypoxia-induced metastasis phenotypes in pancreatic cancer., Data indicate that PYK2 N-terminal domain interacting receptor 1 (Nir1) could induce epithelial-mesenchymal transition by stabilising Snail via the PI3K/Akt/GSK3beta/Snail signalling pathway through binding to CCL18., our results had revealed that Notch-1 could participate in the invasion and metastasis of esophageal carcinoma through EMT via Snail, Gli-1 expression increased markedly, and was closely associated with increased Snail expression and decreased E-cadherin, interaction between DNA-PKcs and Snail1 might be an effective strategy for sensitizing cancer cells and inhibiting tumor migration, Snail mediates TGF-beta1-induced down-regulation of VE-cadherin, which subsequently contributed to TGF-beta1-decreased trophoblast cell invasion., TGF-beta1 resulted in epithelial-mesenchymal transition in bronchial epithelial cells, characterized by decrease in E-cadherin expression and the increase in vimentin and alpha-smooth muscle actin expression, and the associated increase in Snail expression., miR-200/ZEB forms a tristable circuit that acts as a ternary switch, driven by miR-34/SNAIL, that is a monostable module that acts as a noise-buffering integrator of internal and external signals., Co-stimulation with EGF and TGFB1 results in rapid and robust ERK1/2 activation and induces persistent high expression of Snail protein., Snail1 expression controlled migration as well as proliferation of cocultured colon cancer cells in a paracrine manner., silencing gene SNAI1 inhibits expression of properties that are associated with the malignant phenotype of MCF-7 cells and reverses the epithelial-mesenchymal transition process by regulating relevant target gene E-cadherin., AKT/beta-catenin/Snail signaling pathway is mechanistically associated with cancer stem cell-like properties and epithelial-mesenchymal transition features of A549/CDDP cells, and thus, this pathway could be a novel target for the treatment of NSCLC., The functional germline variant c.353T>C (p.Val118Ala) of Snai1 confers consistently decreased risks of lung cancer and COPD, and this variant affects lung cancer risk through a mediation effect of COPD., Snail1 may act more critically in E-cadherin-positive gastroesophageal junction (GEJ) adenocarcinoma tumors, Sustained snail expression plays an essential role in glial-mesenchymal transition after irradiation., These results suggest that Snail could be one of the attractive targets for the development of therapeutic strategies in Head and neck squamous cell carcinoma, MUC1 and SNAIL were overexpressed in human renal sarcomatoid carcinomas., High TWIST1 and SNAI1 mRNA expression was associated with poor overall survival in human colorectal cancer., SNAIL expression was attenuated by knockdown of EGR-1, but upregulated by ectopic expression of EGR-1., grade. It is concluded that increased SNAIL levels in advanced Prostate cancer are associated with low expression of syndecan 1., Snail is required for the maintenance of stem cell-like phenotype in pancreatic cancer., High Snail-1 and Cx43 levels accompanied high motility and nanomechanical elasticity of a prostate cancer cell line., Snail induces the expression of microRNA-146a (miR-146a) through the beta-catenin-TCF4 complex., results suggest that E-cadherin loss promotes SNAI1 expression that controls the aggressiveness of prostate cancer cells, The expression of epithelial markers E-cadherin and Zona occludin-1 were down-regulated, whereas mesenchymal markers alpha-smooth muscle actin and fibronectin were up-regulated in Snail expression vector transfected retinal pigment epithelial cells., Stabilization of Snail by HIF-1alpha and TNF-alpha is required for hypoxia-induced invasion in prostate cancer cells., SNAI1, SNAI2, SNAI3 show unequal oncogenic potential, strictly correlating with their ability to promote epithelial-to-mesenchymal transition., Findings suggest cooperation between AR and RUNX in the stimulation of oncogenes such as SNAI2, which might be targeted for individualized prostate cancer therapy., Snail cooperates with LSD1 to repress PTEN in a PARP1-dependent manner., Although there are many kinds of C2H2-type ZFs which have the same fold as Snail, nuclear import by direct recognition of importin beta is observed in a limited number of C2H2-type zinc-finger proteins such as Snail, SNAIL1 overexpression is associated with tumor growth, metastasis, and chemoresistance in gastric cancer., Reexpression of Let-7g microRNA inhibits the proliferation and migration via K-Ras/HMGA2/snail axis in hepatocellular carcinoma., PGE2 activates Akt/NF-kappaB signaling and then upregulates Snail via the EP4R/EGFR to promote migration and invasion in hepatoma cells., Data indicate that zinc finger protein SNAIL modulates ribosomal protein S6 kinase 1 (RPS6KB1)/HIF-1alpha/protein kinase 2 (PKM2) signaling pathway through miR-128., These observations support a signaling network among JNKs, Smads, Snail1, and cortactin to regulate the invasion of MDA-MB-231 cells embedded in 3D collagen I, which may be targeted during screening of anti-invasion reagents., This is the first report showing the transcriptional regulation of hPLSCR1 expression by Snail TF and its possible implications in cancer progression., Snail and Slug mediate tamoxifen resistance in breast cancer cells through activation of EGFR-ERK independent of epithelial-mesenchymal transition., overexpression of Snail in PDAC cells increased SCF levels, and the media conditioned by Snail-expressing PDAC cells promoted mast cell migration., an analysis of human sarcomas shows that, contrarily to epithelial tumors, these neoplasms display high Snail1 expression., Data revealed that upregulated SNAI1 accelerates glioma progression and suppresses the expression of miR-128, which can oppose SNAI1's effect and modulate SP1 expression., High Snail expression is associated with gastrointestinal stromal tumor metastasis., Data demonstrate that inhibitation of Snail-induced Nanog expression during EMT., PAK1 and Snail1 are involved in the formation of estrogen-independent phenotype of breast cancer cells showing the potential role of both proteins as markers of hormone resistance of breast tumors., miR-199a suppressed the translation of SNAI1, a transcriptional repressor that plays a role in epithelial-to-mesenchymal transition, by targeting the sequence within the 3'UTR of the SNAI1 mRNA, and reduced the protein level of SNAI1., Taken together, these data suggest that miR-375 may be negatively regulated by Snail and involved in gastric cancer cell migration and invasion potentially by targeting JAK2., Knockdown of Akt2 using siRNAs or the PI3K inhibitor Ly294002 inhibited TGF-beta1-induced phosphorylation of GSK3beta and expression of Snail1, The Shh pathway promotes the CSC self-renewal in ATC cell lines by Gli1-induced Snail expression., this is the first study to demonstrate that bFGF can induce EMT via AKT/GSK-3beta/Snail signaling pathway in prostate cancer cells., data suggest that ERK2 isoform activation by Snail in aggressive breast cancer cells leads to EMT associated with increased cell migration and decreased cell adhesion, The PKC/GSK-3beta signaling pathway controls both the stability and transcription of Snail, which is crucial for epithelial-mesenchymal transition induced by EGF in PC-3 and A549 cells., SNAIL1 expression during breast cancer metastasis was transient and forced transient, but not continuous. SNAIL1 expression in breast tumors was sufficient to increase metastasis., Snail regulates the motility and invasiveness of oral cancer cells via RhoA/Cdc42/p-ERM pathway., A significant correlation between expression of Snail1, Snail2 and Zeb1 with miR-200f repression and CpG miR-200c-141 promoter methylation was detected in endometrial carcinosarcomas., The PKD1-FBXO11-SNAIL axis is a mechanism of posttranslational regulation of epithelial-mesenchymal transition and cancer metastasis., results identify EPHB3 as a novel target of SNAIL1 and suggest that disabling EPHB3 signaling is an important aspect to eliminate a roadblock at the onset of EMT processes., This finding demonstrates the upregulated expression of the key epithelial- to-mesenchymal transition (EMT) regulator Snail and that it mediated EMT activation and cell invasion by XBP1., Transcription factor snail regulates tumor necrosis factor alpha-mediated synovial fibroblast activation in the rheumatoid joint., SNAI1 3'UTR overexpression regulated key epithelial-to-mesenchymal transition (EMT) markers, including SNAI1, Vimentin, and E-cadherin, and functioned as a sponge for multiple migration-/invasion-related microRNAs (miRNAs) in RMUG-L cells, these findings revealed that macrophages that have infiltrated tumors may induce epithelial-mesenchymal transition of HCC cells via the IL-8 activated JAK2/STAT3/Snail pathway., Identified a novel binding site for c-Jun in the promoter of the Snail1 gene and report that the activation of the TGFbeta-TRAF6-p38 MAPK pathway promotes both c-Jun expression and its activation via p38alpha-dependent phosphorylation of c-Jun at Ser63., Snail1 expression in human tumor-derived CAF was associated with an ability to organize the ECM., Results suggest that Snai1 is a key factor that triggers ESCs exit from the pluripotency state and initiate their differentiation processes., The overexpression of RKIP can enhance the sensitivity of human gastric cancer cells to cisplatin, which may be achieved via the NF-kappaB/Snail signaling pathway., silencing SNAIL can sensitize TRAIL-induced apoptosis in HCC cells by upregulating p53 protein and by regulating related genes of the NF-kappaB pathway such as Bcl-xL, survivin and Raf-1., results suggest that a combined Runx2/Snail expression could be used as a new significant prognostic biomarker for patients with breast cancer., HMG20A together with LSD1 are required for SNAI1-dependent repression of epithelial genes., hypoxia promotes HO-8910PM ovarian cancer cell traffic through 3D matrix via Snail-mediated MT1-MMP upregulation, a possible molecular mechanism of ovarian cancer cell invasion under hypoxia, High SNAIL1 expression is associated with gastric cancer., This study shows that TGF-alpha uses common and divergent molecular mediators to regulate E-cadherin expression and cell invasion., Results indicate that poly(ADP-ribose) polymerase-1 (PARP-1) controlled transcription factor Snail expression at transcriptional level in cells exposed to doxorubicin., data support a Snail1-dependent mechanism of BBB disruption and penetration by meningeal pathogens., ILK may have an important role in the progression of NSCLC, possibly through up-regulation of Snail and MRP1., Hypoxia-induced endothelial to mesenchymal Transition is mediated by HIF1alpha through direct targeting of SNAIL., the expression levels of HIF1a, Snail and Ecadherin were correlated with clinical pathological factors in human ovarian cancer., LASP-1 associated with UHRF1, G9a, Snail1 and di- and tri-methylated histoneH3 in a CXCL12-dependent manner based on immunoprecipitation and proximity ligation assays, Data show that 3'UTR of Snail1 is a direct target for miR-153 and both expression are inversely correlated with each other in pancreatic ductal adenocarcinoma. HCC cells., osthole suppresses the EMT-mediated metastatic ability in prostate cancer by inhibiting snail signaling and miR-23a-3p, loss of Snail1 causes changes in the actin cytoskeleton, decreases cell-substrate adhesion, and increases cell-cell adhesion., We found that TWIST1, SNAIL and SLUG are overexpressed in endometriosis, A dynamic alteration in TERT promoter occupancy by Snail and c-Myc is the mechanistic basis for TGF-beta-mediated regulation of TERT., findings suggest that increased expression levels of ZEB1 and Snail1 in FECD cells were responsible for an increased responsiveness to TGF-beta present in the aqueous humor and excessive production of ECM, Data suggest that activin A up-regulates SNAIL expression via ALK4/ACVR1B-induced SMAD signaling in trophoblast cells; elevated SNAIL contributes to up-regulation of MMP2 expression which plays key role in promoting trophoblast cell invasion., Snail and Slug expression were up-regulated in the ectotopic endometrium of adenomyosis patients compared with normal endometrium., The downregulation of ZEB1, Twist1, and Snail1 reduces the invasive properties of uveal melanoma cells, and the elevated mRNA levels of ZEB1 and Twist1 are associated with a more aggressive clinical phenotype in uveal melanoma samples., Snail and DAB2IP interact to regulate EMT, invasion and metastasis in colorectal cancer, DDR2 plays an important role in promoting hepatocellular carcinoma cell invasion and migration by stabilizing SNA1., The strong association between Snail expression and lymph node metastasis suggests that Snail mRNA can be used as an adjunct to lymph node positivity to predict survival in pancreatic cancer., loss of Scribble-induced HuR translocation mediates the accumulation of Snail via activation of the p38 MAPK pathway., SNAI1 and SNAI2 - transcriptional master-regulators of epithelial-mesenchimal transition, GM130 upregulated expression of the key epithelial-mesenchymal transformation regulator Snail (SNAI1), which mediated EMT activation and cell invasion by GM130., The present study was performed using LNCaP and PC3 cell lines, in which the expression levels of SNAIL1 were increased or silenced through the use of lentiviral vectors., When Notch-downstream pathways were analyzed, the study detected an increase in glycogen synthase kinase 3 beta phosphorylation and inactivation that facilitates Snail1 nuclear retention and protein stabilization., Downregulation of tumor suppressing STF cDNA 3 promotes epithelial-mesenchymal transition and tumor metastasis of osteosarcoma by the Wnt/GSK-3beta/beta-catenin/Snail signaling pathway.,
SP_COMMENT function:Seems to be involved in embryonic mesoderm formation. Binds to 3 E-boxes of the E-cadherin gene promoter and represses its transcription., similarity:Belongs to the snail C2H2-type zinc-finger protein family., similarity:Contains 4 C2H2-type zinc fingers., tissue specificity:Expressed in a variety of tissues with the highest expression in kidney.,