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BRMS1L promotes chemotherapy sensitivity by inhibiting autophagy in breast cancer

ABSTRACT: BRMS1L (Breast cancer metastasis suppressor 1 like), a component of Sin3A-histone deacetylase (HDAC) co-repressor complex, has been shown to provide an epigenetic regulation ofWnt signal pathway and act as a metastasis suppressor in breast cancer. However, the role of BRMS1L in the progression and chemosensitivity has not been explored. In the present study, we for the first time showed that reduced BRMS1L expression correlates with poor response to neoadjuvant chemotherapy and poor prognosis in patients with breast cancer. Additionally, chemoresistant breast cancer cells exhibited decreased BRMS1L expression and increased autophagy levels. Furthermore, ectopic expression of BRMS1L significantly enhanced chemotherapy sensitivity via inhibiting protective autophagy in breast cancer cells. In vivo, the experiments in nude mice showed that BRMS1L strengthened the chemotherapy effects on xenografts. Collectively, these results revealed that BRMS1L enhances chemotherapy sensitivity via inhibiting autophagy. Our findings uncover a novel role of BRMS1L in drug sensitivity and highlight the potential clinical application of BRMS1L in the treatment of breast cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE306386 | GEO | 2025/10/21

REPOSITORIES: GEO

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BRMS1L promotes chemotherapy sensitivity by inhibiting autophagy in breast cancer

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