Cancer management and research · 2026
LRRC32 Mediates Resistance to Everolimus in Hormone Receptor-Positive, HER2-Negative Breast Cancer.
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Wang Liguang, Chen Xue, Li Xiaojiao, Wang Yu, Shen Rong
Аннотация
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.
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.