First-pass extracted concept

E-cadherin

Candidate: concept label2 source documents3 linked claims

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Aliases

CDH1

Evidence Snippets

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

Evidence 1Source 1DOI PubMedprovenance

loss of junction protein E-cadherin

Evidence 2Source 2DOI PubMedprovenance

Supporting Sources

Source 1primary paper2026MEDDOI PubMed

1 evidence snippet 2 linked claims Claim 1 Claim 2

Source 2primary paper2015OncotargetDOI PubMed

1 evidence snippet 1 linked claim Claim 1

Linked Claims

Claim 1mechanistic modelsupports2026Source 1DOI PubMed

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 2mechanistic regulationsupports2026Source 1DOI PubMed

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.

Claim 3mechanistic associationsupports2015Source 2DOI PubMed

The increased EMT phenotypes observed with vimentin overexpression in MCF7 cells were associated with increased β1-integrin and loss of E-cadherin.