VIM
Overview
VIM encodes vimentin, a type III intermediate filament protein and classic marker of mesenchymal identity used to assess epithelial-to-mesenchymal transition (EMT). Elevated vimentin expression is a downstream readout of SEMA7A-driven EMT in gallbladder cancer.
Alterations observed in the corpus
- Upregulated in GBC xenograft tumors co-injected with gallbladder fibroblasts (GFs) vs GBC-SD cells alone; SEMA7A knockdown in GFs reduced vimentin expression in co-injection models (n=6 per group). Functions as an in vivo EMT readout in the SEMA7A/ITGB1/AKT1/EP300 axis study. PMID:24997986
Cancer types (linked)
- Gallbladder cancer (GBC): VIM upregulation marks CAF-driven EMT in the desmoplastic tumor microenvironment. PMID:24997986
Co-occurrence and mutual exclusivity
- Co-upregulated with CD44, EPCAM, ALDH1A1 (stemness markers) and SNAI1, ZEB1 (EMT TFs) downstream of SEMA7A paracrine signaling; downregulation of CDH1 (E-cadherin) accompanies VIM upregulation. PMID:24997986
Therapeutic relevance
- VIM upregulation reversed by SEMA7A knockdown in GFs in vivo; upstream blockade (verteporfin, LY294002, C646) also reduces EMT markers including vimentin in vitro. PMID:24997986
Open questions
- VIM is used as a functional readout rather than a genetic driver in the citing study; somatic alterations in VIM are not reported.
Sources
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