ArticleFrontiers in genetics2025
BRMS1L promotes chemotherapy sensitivity by inhibiting autophagy in breast cancer.
Article in Frontiers in genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
7 authors.
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Abstract
Chemoresistance remains a crucial obstacle in breast cancer therapy. The mechanisms underlying chemoresistance need to be explored urgently and in depth. Breast cancer metastasis suppressor 1 like (BRMS1L), a core component of the Sin3A-histone deacetylase (HDAC) co-repressor complex, has been reported to suppress breast cancer metastasis through epigenetically regulating the Wnt signal pathway. However, whether BRMS1L could regulate chemosensitivity has not been explored. Herein, we found that higher BRMS1L expression was significantly correlated with increased chemotherapy sensitivity and better prognosis in patients receiving neoadjuvant chemotherapy.
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