ArticleIn vitro cellular & developmental biology. Animal2026
Oncogenic role and potential mechanisms of MYO1B in breast cancer.
Article in In vitro cellular & developmental biology. Animal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Myosin IB (MYO1B), a member of the type I myosin family, is overexpressed in various tumor tissues. MYO1B facilitates tumor progression by regulating cellular proliferation, migration, and the epithelial-mesenchymal transition (EMT). However, the precise function of MYO1B in breast cancer (BRCA) is still not well understood. We analyzed MYO1B expression, prognostic significance, immune infiltration, and its correlation with drug resistance in BRCA using meta-analysis and public databases. Functional assays in BRCA cells were performed to evaluate the effects of MYO1B on cell proliferation, apoptosis, and sensitivity to tamoxifen and palbociclib. MYO1B mRNA levels showed no significant difference between BRCA and normal tissues, whereas MYO1B protein was upregulated in tumor tissues. High MYO1B expression was associated with poor prognosis in BRCA patients. Functionally, MYO1B promoted BRCA cell proliferation, inhibited apoptosis, and increased resistance to tamoxifen and palbociclib. Mechanistically, MYO1B activated the Pi3k-AKT signaling pathway. Our study suggests that MYO1B promotes the progression of BRCA and may serve as a new target for overcoming endocrine therapy resistance.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.