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Symbol SNAI1 contributors: mct - updated : 05-05-2018
HGNC name snail homolog 1 (Drosophila)
HGNC id 11128
Location 20q13.13      Physical location : 48.599.512 - 48.605.418
Synonym name
  • snail 1 (drosophila homolog), zinc finger protein
  • protein sna
  • Synonym symbol(s) SLUG2, SNAI, SNAIL, SNA, SNAH, SLUGH2, SNAIL1, dJ710H13.1
    TYPE functioning gene
    STRUCTURE 5.89 kb     3 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    regulatory sequence Promoter
    Binding site   silencer
    text structure
  • A 5'-CACCTG-3' box in the promoter represses its activity
  • MAPPING cloned Y linked N status provisional
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    3 - 1708 29 264 - 2001 11245431
    Type widely
       expressed in (based on citations)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Reproductivefemale systembreast    Homo sapiens
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Epithelialabsorptive excretoryglandular  
    cell lineage
    cell lines stromal fibroblasts
    at STAGE
    physiological period fetal, pregnancy
    Text tissues, highly in kidney
  • N-terminal SNAG domain, important for the repressor activity, required for interaction with KDM1A, and that resembles a histone H3-like structure and functions as a molecular hook for recruiting KDM1A to repress gene expression in metastasis
  • three classic and one atypical zinc finger motifs
  • C-terminal tandem zinc finger motifs
    interspecies ortholog to zinc finger protein Drosophila snail 1
    homolog to murine Snai1 (87.5pc)
    homolog to rattus Snai1 (89pc)
  • snail C2H2-type zinc-finger protein family
  • CATEGORY regulatory , transcription factor
    SUBCELLULAR LOCALIZATION     intracellular
    basic FUNCTION
  • formation of mesoderm and neural crest, down regulating the expression of ectodermal crest
  • repressor of CDH1 in breast cancer
  • key regulator of epithelial-mesenchymal transition
  • regulating CDKN1A expression in cooperation with TWIST1 and TCF3
  • first cue corrected by retinoic acid in the presomitic mesoderm to ensure synchronized bilateral segmentation
  • involved in renal tubular epithelial-mesenchymal transition
  • acting as a major effector downstream of HMGA2 for induction of EMT, as SNAI1 knock-down partially reverses the effect of HMGA2 on mesenchymal differentiation
  • acting as a repressor that down-regulates the expression of CYP19A1 in normal breast tissue by suppressing the function of promoter I.3
  • acts downstream of FGFR3 signaling in chondrocytes, regulating both Stat and MAPK pathways
  • combined expression of SNAI2 and SNAI1 is required for endothelial-to-mesenchymal transition in cardiac cushion morphogenesis
  • its activation is involved in a positive feedback stimulation of the Wnt pathway
  • controls the balance between bone formation and bone resorption by controlling osteoblast differentiation
  • repressing the transcription of the osteoblast differentiation factor RUNX2 and the vitamin D receptor genes in osteoblats
  • in colorectal cancer tissues, regulates expression of IL8 and other genes to induce cancer stem cell activities
  • SNAI1, SNAI2, and TCF3 can promote collective migration during branching morphogenesis of mammary epithelial tissues through key regulators of EMT (epithelial-mesenchymal transition)
  • plays a critical role in TGFB1-induced EMT in human RPE cells, which provides deep insight into the pathogenesis ofproliferative vitreoretinopathy
  • central regulator of epithelial cell adhesion and movement in epithelial-to-mesenchymal transitions (EMTs) during embryo development, and a process reactivated during cancer metastasis
  • could inhibit the expression of the vitamin-D gene receptor (VDR), and inhibits 1,25(OH)-D&
  • 8323; action in osteosarcoma
  • transcriptional factor essential for triggering epithelial-to-mesenchymal transition
  • SMAD3 and SNAI1 have circadian rhythm and circadian expression of SMAD3 depends on CLOCK/ARNTL
  • regulator of EMT that represses CDH1 transcription through its interaction with proximal E-boxes in the promoter region of target genes
  • like MMP3, the transcriptional activities of SNAI1 and SNAI2 genes were also negatively associated with the DNA methylation status of the first intron regions
  • SNAI1, SNAI2 genes are regulated by DNA methylation and the DNA methylation of first intron were associated with their transcription in EMT/MET processes
  • SNAI1 -mediated suppression of OTUD7A may have a key role in hepatocellular carcinoma malignancy
  • CELLULAR PROCESS nucleotide, transcription, regulation
    text transcriptional repressor
    a component
  • forming a complex with SMAD3 and SMAD4 to promote TGFbeta-mediated epithelial-mesenchymal transition
  • formation of a SNAI1–KDM1A–RCOR1 ternary complex critical for the stability and function of these proteins
    DNA binding to 3 E-boxes of the E-cadherin gene promoter and repressing its transcription
    small molecule metal binding,
  • ions Zn2+
  • protein
  • interacting with VDR, CDH1 and TCF8 in carcinogenesis (overexpression of SNAI1 repressing VDR and CDH1)
  • interacting with VDR and TCF8 in colorectal cancer (loss of VDR and TCF8 and presence of SNAI1 is predictor of poor clinical prognosis)
  • interacting with PEBP1 (novel component of the SNAI1 transcriptional regulatory network important for the progression and metastasis of cancer)
  • interacting with PRMT5, effector recruited to SNAI1 through an interaction with JUB that functions to repress the SNAI1 target gene, CDH1
  • interacting with SUZ12 (SNAI1 increases the binding of SUZ12 to the CDH1 promoter and the trimethylation of lysine 27 in histone H3)
  • binding to HMGA2
  • can bind to an E-box of the myosin Va promoter and induce its activity, which indicates that SNAI1 might act as a transcriptional activator
  • interacted with histone lysine-specific demethylase 1 (KDM1A)(SNAG domain of SNAI1 and the amine oxidase domain of KDM1A were required for their mutual interaction)
  • interaction with the KDM1A/RCOR1 complex is critical for the stability and function of SNAI1
  • SNAI1 controls ZEB1 expression at multiple levels and acts cooperatively with TWIST1 in the ZEB1 gene transcription induction
  • PTK2 is a novel regulator of SNAIL1-dependent epithelial-mesenchymal transition in embryonic cells
  • NOTCH1 intracellular domain (NICD) is a novel SNAIl-binding partner, and this interaction was found to induce ubiquitination and MDM2-dependent degradation of SNAI1, and NOTCH1 binds and induces degradation of SNAIl in hepatocellular carcinoma
  • SNAI1 enhances the binding of AKT2 to the E-cadherin (CDH1) promoter and AKT2 interference prevents SNAI1 repression of CDH1 gene
  • PRDX1 regulated the expression of two E-cadherin transcriptional repressors, SNAI1, SNAI2
  • regulates MYOD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis
  • AXIN2 acts as a potent promoter of carcinoma behavior by up-regulating the activity of the transcriptional repressor, SNAI1, inducing a functional epithelial-mesenchymal transition (EMT) program and driving metastatic activity
  • PRKD1 efficiently interacts with SNAI1 in nuclei
  • binds to E-boxes in the ESRP1 promoter, causing repression of the ESRP1 gene
  • down-regulates PTGS2
  • SNAI1 inhibits NOTCH1 intracellular domain mediated transcriptional activation via competing with MAML1
  • SNAI1 binds to the promoter of the OTUD7A gene and mediates the direct consequence of OTUD7A repression
  • DYRK2 regulates cancer invasion and metastasis by degrading SNAI1
  • ETV1 promotes SNAI1 expression to induce EMT-like metastatic progression in gastric cancer
  • FBXL5 is a novel SNAI1 ubiquitin ligase
  • SNAI1 regulates heterochromatin transcription through LOXL2, thus creating the favorable transcriptional state necessary for completing EMT (epithelial-to-mesenchymal transition)
  • SNAI1 C2H2-type zinc-finger (ZF) domain functions both as a nuclear localization signal which binds to KPNB1 directly and as a DNA-binding domain
  • SNAI1-DLL4/NOTCH1 axis controls embryonic vascular development
  • SNAI1 recruits RNF2 to mediate transcriptional repression and cell migration in pancreatic cancer cells
  • PCDH9 is a novel regulator of EMT by increasing the activity of GSK3B and inhibiting SNAI1
  • HMG20A together with KDM1A are required for SNAI1-dependent repression of epithelial genes and for TGFB1-triggered EMT
  • VANGL1 induced the expression of the epithelial-mesenchymal transition (EMT) markers (N-cadherin, ZEB1, ZEB2, SNAI1 and SNAI2) as well as the glioma stemness markers (CD133, ALDH1 and EPHB1)
  • represses TDGF1 gene by direct transcriptional interaction and it co-ordinately regulates likely cell fate decisions during development and could be causal of cancers)
  • important role for KDM8 in breast cancer through the regulation of SNAI1
  • MAPK14 mediates epithelial-mesenchymal transition by regulating SUP20TH and SNAI1 in Head and Neck squamous cell carcinoma
  • KRT18 critically contributes to initiating TGFB1-induced EMT via the SMAD2/3 -mediated regulation of SNAI1, SNAI2 expression in breast epithelial cells
  • ANXA1 promotes the proliferation of esophageal squamous cell carcinoma (ESCC) cells, and increases the expression of SNAI1, whereas it inhibits that of CDH1, thus enhancing the migration and invasion of ESCC cells
  • SPSB3 is a novel E3 ligase component that targets SNAI1 into polyubiquitination and degradation in response to GSK3B phosphorylation of SNAI1
  • enhanced PAPSS2/VCAN sulfation axis is essential for SNAI1-mediated breast cancer cell migration and metastasis
  • LAMP2 attenuates EMT by suppressing SNAI1 expression in hepatocellular carcinoma (HCC)
  • FSCN1 promote Epithelial-mesenchymal transition (EMT) through SNAI1 in ovarian cancer cells
  • SNAI1 elicits collective migration in squamous cell carcinoma by inducing the expression of a tight junctional protein, CLDN11
  • cell & other
    induced by POU2F1 (POU2F1 induced the expression of TWIST1, SNAI1, SNAI2 and ZEB1 genes which are involved in the regulation of epithelial-to-mesenchymal transition (EMT)
    Other expression of Snail1 gene can be regulated by its product by an inhibitory feed-back control
    regulated by TGFB1 at the transcription and protein degradation levels
    regulated by protein degradation, and GSK3B has been found to play an important role in degradation
    LATS2 kinase is a novel regulator of SNAI1 protein level, subcellular localization, and thus, activity
    DNA methylation is one of the molecular mechanisms regulating SNAI1 and SNAI2 genes during EMT/MET process
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in breast cancer with poor survival
    constitutional     --over  
    in the tubular cells of the kidney on the obstructed side
    constitutional     --low  
    in breast cancer tissue further suggests a cancer-protective role for this protein in normal breast tissue
    constitutional     --over  
    aberrantly upregulated in thanatophoric versus normal cartilages from stillborns
    tumoral     --over  
    in osteosarcoma
    Variant & Polymorphism
    Candidate gene
    Therapy target
    may be therapy target for breast cancer
    strategies to suppress SNAIl-mediated signaling may lead to the better action of 1,25(OH)-D₃ as an anti osteosarcoma treatment
    potential therapeutic target to block tumour progression (its silencing effectively suppresses tumour growth and invasiveness)
    miscelleaneousurinarychronic kidney disease
    GSK3B-SNAI1 axis may be a suitable target for the treatment of chronic kidney diseases
    SNAIl activity may likely be considered a target for achondroplasia therapies
    chemical compounds that mimic the structure of the SNAG domain of SNAI1 may hold great promise for inhibiting the function of SNAI1 in mediating EMT induction and cancer metastasis
    specific inhibition of SNAIl may provide a new approach to treat and prevent proliferative vitreoretinopathy
    expressed in the right side of LPM in the mouse