BCL-B Promotes Lung Cancer Invasiveness by Direct Inhibition of BOK.

ABSTRACT: Expression of BCL-B, an anti-apoptotic BCL-2 family member, is correlated with worse survival in lung adenocarcinomas. Here, we show that BCL-B can mitigate cell death initiation through interaction with the effector protein BOK. We found that this interaction can promote sublethal mitochondrial outer membrane permeabilization (MOMP) and consequently generate apoptosis-flatliners, which represent a source of drug-tolerant persister cells (DTPs). The engagement of endothelial-mesenchymal-transition (EMT) further promotes cancer cell invasiveness in such DTPs. Our results reveal that BCL-B fosters cancer cell aggressiveness by counteracting complete MOMP.

SUBMITTER: Ramesh P 

PROVIDER: S-EPMC11853756 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature