SNAI1
Overview
SNAI1 encodes Snail, a zinc-finger transcription factor that represses E-cadherin (CDH1) expression and is a master regulator of epithelial-to-mesenchymal transition (EMT). In gallbladder cancer, SNAI1 transcription is epigenetically activated downstream of a paracrine SEMA7A/ITGB1/AKT1/EP300 signaling cascade driven by cancer-associated fibroblasts.
Alterations observed in the corpus
- Transcriptionally upregulated in GBC cells downstream of SEMA7A/ITGB1/AKT1/EP300 signaling; p300 occupancy and H3K27ac at the SNAI1 promoter increased by recombinant SEMA7A, abrogated by p300 S1834A mutation; promoter H3K27ac blocked by C646 (p300 inhibitor). PMID:24997986
Cancer types (linked)
- Gallbladder cancer (GBC): SNAI1 is an EMT effector activated downstream of stromal SEMA7A paracrine signaling via an AKT1/EP300 epigenetic axis. PMID:24997986
Co-occurrence and mutual exclusivity
- Co-upregulated with ZEB1 as EMT drivers downstream of SEMA7A signaling in GBC; both regulated via p300-dependent H3K27 acetylation. PMID:24997986
Therapeutic relevance
- SNAI1 induction can be blocked by targeting upstream nodes: verteporfin (YAP inhibitor, blocks SEMA7A induction in GFs), LY294002 (PI3K inhibitor), or C646 (p300 inhibitor). PMID:24997986
Open questions
- Whether SNAI1 itself bears somatic mutations in GBC was not assessed in the citing study, which is mechanistic rather than genomic.
Sources
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