ArticleCancer management and research2026
LRRC32 Mediates Resistance to Everolimus in Hormone Receptor-Positive, HER2-Negative Breast Cancer.
Article in Cancer management and research, 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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5 authors.
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Abstract
Aim: Everolimus is approved for hormone receptor-positive, HER2-negative breast cancer, but resistance mechanisms remain incompletely understood. This study aimed to investigate the functional role of LRRC32 in mediating Everolimus resistance using patient-derived organoid (PDO) models of this breast cancer subtype. Materials and Methods: Everolimus-resistant and sensitive breast cancer organoids were established from patient-derived tumor tissues. RNA sequencing was performed to compare expression profiles. In vitro functional assays were conducted, including LRRC32 overexpression and shRNA-mediated knockdown, MTT cell viability assay, flow cytometric apoptosis detection, and flow cytometric cell cycle analysis. Results: RNA sequencing identified significant LRRC32 upregulation in resistant cells with a fold change of 180.46 (p < 0.001). LRRC32 overexpression reduced apoptosis and enhanced cell survival, whereas knockdown increased apoptosis. Cell cycle analysis showed that LRRC32 knockdown in resistant cells significantly increased the G1-phase fraction, hindering G0/G1-to-S transition. Conclusion: Our findings suggest that LRRC32 plays a pivotal role in modulating the sensitivity of breast cancer cells to Everolimus.
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