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SNAI1 transcriptional activation by FOXF1 induced epithelial-mesenchymal transition and promoted invasion and metastasis of colorectal cancer cells.
Findings suggest proteasome 26S subunit non-ATPase 14 (PSMD14) as a deubiquitinating enzyme to regulate Snail transcription factor (SNAIL) at the post-translational level and provide a promising therapeutic strategy against tumor metastasis of esophageal cancer.
-box and WD repeat domain containing 7 (FBW7) silencing stabilized Snail protein and induced epithelial-to mesenchymal transition (EMT), and acquisition of migration and invasion properties in non-small cell lung cancer (NSCLC).
SNAI1 is known to promote epithelial to mesenchymal transition by repressing E-cadherin expression, but it needs an intact PRC2 to act this function. Alterations of this process could contribute to the complex etiology of nsCL/P.
Activation of GPER can suppress the migration and invasion of OS cells via FBXL5-mediated post-translational down regulation of Snail. It suggested that targeted activation of GPER might be a potent potential therapy approach to overcome the metastasis of OS patients
The results strongly suggest that the integrated pathway of TGF-beta/Snail with TNFalpha/NF-kappaB may be the principal axis that links cancer cells to their microenvironment during the epithelial-mesenchymal transition process and results in poor prognosis in colorectal cancer patients.
Phosphorylation of Ser is essential for Snail1 to be recognized by FBXO31 which mediates the ubiquitination and degradation of Snail1.
Data suggest that SNAI1 is a key regulator of FGF2-dependent mesenchymal transition in corneal endothelium, with ZEB1 regulating type I collagen expression and CDK2 regulating cell proliferation. (SNAI1 = snail family transcriptional repressor-1; FGF2 = fibroblast growth factor-2; ZEB1 = zinc finger E-box binding homeobox-1 protein; CDK2 = cyclin dependent kinase-2)
Smad3-mediated recruitment of SETDB1 controls Snail1 expression and epithelial-mesenchymal transition in ductal breast carcinoma.
Snail1 gene silencing effectively improved the drug sensitivity of MMCs to bortezomib chemotherapy.
Up-regulation of long non-coding RNA XLOC_010235 regulates epithelial-to-mesenchymal transition to promote metastasis by associating with Snail1 in gastric cancer.
Study provides evidence that genetic variants in SNAI1 and TWIST1 are associated with breast cancer (BC) and ovarian cancer (OC) susceptibility and suggests a synergistic effect of those related loci on BC/OC risk.
Ovarian cancer patients show elevated serum CXCL1/2, which correlates with Snail expression, myeloid-derived suppressor cells infiltration, and short overall survival. Snail induces ovarian cancer progression via upregulation of CXCR2 ligands and recruitment of myeloid-derived suppressor cells.
Data suggest that HOP homeobox HOPX (HOPX) acts as a tumour suppressor via the epigenetic regulation of snail family transcription factors (SNAIL) transcription and a prognostic biomarker for nasopharyngeal carcinoma (NPC) metastasis and therapeutic target for NPC treatment.
The authors identify SNAI1 as the key Epithelial-Mesenchymal Transition transcriptional factor required for the specification of definitive endoderm.
Snail functions as a metabolic switch between aerobic glycolysis and pentose phosphate pathway by repressing PFKP, a cancer-specific PFK-1, allowing cancer cell survival under metabolic stress.
At the molecular level, transcription of the adherens junction protein E-cadherin is upregulated on nicotinic acid addition, leading to accumulation of E-cadherin protein at the cell-cell boundary. This can be attributed to nicotinic acid's ability to facilitate the ubiquitination and degradation of Snail1, a transcription factor that represses E-cadherin expression.
Dub3 is identified as a bona fide Snail1 deubiquitinase, which interacts with and stabilizes Snail1.
High SNAIL1 expression is associated with breast invasive ductal carcinoma.
The present study illustrated that downregulation of CDK10 expression activated Snaildriven EMT and consequently promoted glioma metastasis, suggesting that CDK10 may serve as a potential molecular target for glioma therapy.
Impairment in the insulin-Snail1 axis may contribute to non-alcoholic fatty liver disease in obesity.
Increased SNAI1 expression is associated with the development of severe pulmonary hypertension.
Snail knockdown in mouse ovarian cancer cell lines suppresses tumor growth and expression of CXCR2 ligands. Thus, Snail induces ovarian cancer progression via upregulation of CXCR2 ligands and recruitment of myeloid-derived suppressor cells.
CDK4/CDK6-dependent activation of DUB3 regulates cancer metastasis through SNAIL1.
Neutrophils and Snail orchestrate the establishment of a pro-tumor microenvironment in lung cancer.
Nrf2 attenuates Epithelial-mesenchymal transition and fibrosis process by regulating the expression of snail in pulmonary fibrosis.
Pbx-dependent Epithelial-mesenchymal transition programs mediate murine upper lip/primary palate morphogenesis and fusion via regulation of Snail1.
a Snail1-ATGL axis that regulates adipose lipolysis and fatty acid release, is reported.
A20 promotes metastasis of aggressive basal-like breast cancers through multi-monoubiquitylation of Snail1.
Metagenomic analysis revealed direct correlation between PPARGC1A, SNAI1, and metastatic lung disease.
both Snail and Slug are able to form binary complexes with either YAP or TAZ that, together, control YAP/TAZ transcriptional activity and function throughout mouse development.
results demonstrate that skeletal stem/stromal cell mobilize Snail/Slug-YAP/TAZ complexes to control stem cell function
these results might suggest that calcineurin inhibitor-induced tubular SNAI1 protein cytoplasmic accumulation, possibly because of impaired SNAI1 proteasomal degradation and nuclear translocation, might be a sign of a diseased profibrotic epithelial phenotype.
Snail1 as a molecular bypass that suppresses the anti-proliferative and pro-apoptotic effects exerted by wild-type p53 in breast cancer
Snail1 deficiency modified the phenotype of pancreatic tumors .
miR-200 promotes the mesenchymal to epithelial transition by suppressing multiple members of the Zeb2 and Snail1 transcriptional repressor complexes, such as Smad2 and Smad5.
show that Snail1-induced fibrosis can be reversed in vivo and that obstructive nephropathy can be therapeutically ameliorated in mice by targeting Snail1 expression
Results suggest that Snai1 is a key factor that triggers ESCs exit from the pluripotency state and initiate their differentiation processes.
During embryonic stem cell differentiation, an endogenous Wnt-mediated burst in Snail1 expression regulates neuroectodermal fate while playing a role in epiblast stem cell exit and the consequent lineage fate decisions that define mesoderm commitment.
The Snail transcription factor regulates the numbers of neural precursor cells and newborn neurons throughout mammalian life.
While either Snail or Serpent induced a profound loss of epithelial polarity and tissue organisation, Serpent but not Snail also induced an increase in the size of wing discs. Furthermore, the Serpent-induced tumour-like tissues were able to grow extensively when transplanted into the abdomen of adult hosts.
Disruption of Snail expression in follicle stem cells compromises proliferation, but not maintenance. FSCs with excessive Snail expression had increased proliferation and lifespan, accompanied by a moderate decrease inE-cadherin expression (required for adhesion of FSCs to their niche) at the junction between their adjacent cells, indicating a conserved role of Snail in E-cadherin inhibition.
during gastrulation of Drosophila embryos, Sna expression downregulates polarity protein Baz which in turn results in junction disassembly at protein levels.
evidence for mechanosensitivity of cell-cell junctions and implications that myosin-mediated tension can prevent Snail-driven Eepithelial-mesenchymal transitions
Snail can potentiate enhancer activation by collaborating with different activators, providing a new mechanism by which Snail regulates development.
Rapid transcription kinetics and negative autoregulation are responsible for the remarkable homogeneity of snail expression and the coordination of mesoderm invagination.
Study shows that Sna represses transcription of pbl in the mesoderm primordium of D. melanogaster via one or more Sna-binding sites, which are conserved among species of the Drosophila genus, but not in the mosquito, correlating with the different modes of gastrulation in the different genuses.
Complex interactions between cis-regulatory modules in native conformation are critical for Drosophila snail expression.
The Snail repressor positions Notch signaling in the Drosophila embryo.
results show that Sna has a positive regulatory function on sim expression in the presumptive mesectoderm; this positive effect of Sna depends on the Su(H)-binding sites within the sim promoter, suggesting that Sna regulates Notch signaling
snail is required for Drosophila gastrulation and is not replaceable by Escargot or Worniu.
Dorsal activates twist and snail, and the Dorsal/Twist/Snail network activates and represses other zygotic genes to form the dorsoventral axis in Drosophila.
Snail represses Tom expression in the mesoderm and thereby activates Delta trafficking.
The transcription factor Snail1 is essential for tissue separation, enabling paraxial protocadherin (PAPC) to promote tissue separation through novel functions.
Interaction with Snail1/2, and Twist function more generally, is regulated by GSK-3-beta-mediated phosphorylation of conserved sites in the WR domain.
the same E3 ubiquitin ligase known to regulate Snail family proteins, Partner of paired (Ppa), also controlled Twist stability and did so in a manner dependent on the Twist WR-rich domain
data support a Snail1-dependent mechanism of BBB disruption and penetration by meningeal pathogens.
Snail genes lie in regions of extensive paralogy, revealing their common origin through segmental or chromosomal duplication
data suggest that Nrz, in addition to its effect on apoptosis, contributes to cell movements during gastrulation by negatively regulating the expression of Snail-1, a transcription factor that controls cell adhesion
Snail genes not only act as inducers of epithelial-to-mesenchymal transition, but also as more general regulators of cell adhesion and movement.
NF-kappaB and Snail1a coordinate the cell cycle with gastrulation.
The Drosophila embryonic protein snail is a zinc finger transcriptional repressor which downregulates the expression of ectodermal genes within the mesoderm. The nuclear protein encoded by this gene is structurally similar to the Drosophila snail protein, and is also thought to be critical for mesoderm formation in the developing embryo. At least two variants of a similar processed pseudogene have been found on chromosome 2.
, protein snail homolog 1
, snail 1 homolog
, snail 1 zinc finger protein
, snail 1, zinc finger protein
, snail homolog 1
, zinc finger protein SNAI1
, snail like protein
, Protein snail-like protein 1
, snail homolog 1 (Drosophila)
, zinc-finger transcription factor Snail
, protein Xsnail
, protein snail homolog Sna
, protein xSna
, snail protein
, zinc finger protein with snail domain similar to escargot
, transcription factor protein
, snail zinc finger protein
, snail-like protein 1
, snail family zinc finger 1a