First-pass extracted concept

TMBIM1

Candidate: concept label1 source documents5 linked claims
Live refresh every 5sNext refresh in 5s

Aliases

transmembrane BAX inhibitor motif-containing 1

Evidence Snippets

Mounting evidence from large-scale association studies has identified transmembrane BAX inhibitor motif-containing 1 (TMBIM1) as a promising candidate gene in colorectal cancer (CRC) pathogenesis.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1context dependent functionsupports2026Source 1DOIPubMed

TMBIM1 deficiency suppresses growth in normal colonic epithelial NCM460 cells.

Quoted textsource-backed
In normal colonic epithelial cells (NCM460), TMBIM1 deficiency triggered distinct morphological changes and suppressed cellular growth.
Claim 2context dependent functionsupports2026Source 1DOIPubMed

TMBIM1 knockdown enhances proliferation and pro-tumorigenic characteristics in malignant HCT-116 cells.

Quoted textsource-backed
Conversely, in malignant HCT-116 cells, TMBIM1 knockdown paradoxically enhanced proliferation and other pro-tumorigenic characteristics, suggesting context-dependent functions.
Claim 3expression associationsupports2026Source 1DOIPubMed

TMBIM1 expression is reduced in human colon cancer tissues.

Quoted textsource-backed
Our clinical analysis confirmed this association, demonstrating significantly reduced TMBIM1 expression in human colon cancer tissues.
Claim 4mechanistic modelsupports2026Source 1DOIPubMed

Loss of TMBIM1 in MSI-H cells promotes tumorigenesis via E-cadherin suppression and loss of epithelial integrity.

Quoted textsource-backed
We therefore define a context-dependent tumor-suppressive mechanism for TMBIM1, wherein its loss in MSI-H cells promotes tumorigenesis via E-cadherin suppression and the consequent loss of epithelial integrity.
Claim 5mechanistic regulationsupports2026Source 1DOIPubMed

TMBIM1 knockdown is associated with significant down-regulation of E-cadherin/CDH1.

Quoted textsource-backed
Mechanistic investigations further identified E-cadherin (CDH1) as a key downstream effector, showing significant down-regulation following TMBIM1 knockdown.