LEM4 interacts with β-catenin and promotes β-catenin-dependent transcription activity to confers ribociclib resistance in breast cancer cells.

ABSTRACT: Background Ribociclib, a CDK4/6 inhibitor, is a targeted therapy for breast cancer management. However, acquired resistance to ribociclib is a common clinical challenge. This study aimed to investigate the role of LEM-Domain Protein 4 (LEM4), a nuclear envelope protein, in mediating ribociclib resistance in breast cancer cells and elucidate the underlying molecular mechanisms. Methods LEM4 expression was analyzed in breast cancer patient samples and cell lines. Ribociclib-resistant MCF-7 and T47D cell lines were established, and the effects of LEM4 knockdown on drug sensitivity, apoptosis, and β-catenin signaling were evaluated using in vitro cytotoxicity, co-immunoprecipitation, β-catenin transcription activity and in vivo tumor formation assays. Results LEM4 was found to be overexpressed

SUBMITTER: Tang Q 

PROVIDER: S-EPMC12738774 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature