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αB-crystallin enhances radioresistance in basal-like breast cancer cells by suppressing caspase-3 activation.
Article in Science progress. 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
ObjectiveFor most patients with breast cancer undergoing breast-conserving surgery, radiotherapy reduces local recurrence and mortality. However, in basal-like breast cancer, radiotherapy is less effective due to the cells' intrinsic radioresistance. Understanding the molecular mechanism of radioresistance in basal-like breast cancer is crucial for improving treatment and outcomes.MethodsαB-crystallin levels were determined in different breast cancer cell lines, including basal-like breast cancer cell lines (HCC1599, MDA-MB-468, MDA-MB-231) and luminal breast cancer cell lines (MDA-MB-453, BT-474, MCF-7). To further investigate the role of αB-crystallin in breast cancer cells, we utilized short hairpin RNA lentivirus particles to knock down αB-crystallin expression in MDA-MB-231 cells and overexpressed it in MCF-7 cells via lentivirus-mediated delivery of αB-crystallin. Cell migration and invasion were assessed using transwell assays, and radiosensitivity was evaluated via colony formation assays. Flow cytometry was employed to quantify apoptotic cells and western blot was performed to explore the expression levels of invasion and migration-related proteins and apoptotic proteins. The levels of γ-H2AX and the co-localization of αB-crystallin with Caspase-3 in cells were evaluated using immunofluorescence microscopy. Immunoprecipitation followed by western blot was used to detect the interaction of αB-crystallin with Caspase-3.ResultsWe have identified αB-crystallin as a pivotal regulator of migration and radiosensitivity in basal-like breast cancer. Repression of αB-crystallin expression enhanced radiation-induced DNA damage and apoptosis in basal-like breast cancer cells. Moreover, knockdown of αB-crystallin diminished its interaction with Caspase-3, resulting in an amplified activation of Caspase-3 triggered by irradiation, intensified apoptosis, and heightened radiosensitivity in basal-like breast cancer cells.ConclusionsThe overexpression of αB-crystallin not only enhances the migratory capacity of basal-like breast cancer cells but also confers radioresistance to the cells by directly interacting with Caspase-3 and inhibiting its activity. Suppression of αB-crystallin enhances radiation-induced cell death, thereby improving the radiosensitivity of basal-like breast cancer cells.
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