ArticlePloS one2025
Response Gene to Complement 32 promotes cell proliferation and tamoxifen resistance in breast cancer via elevated FoxM1 expression.
Article in PloS one, 2025. 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
Despite the high sensitivity of estrogen receptor positive (ER+) breast cancer to endocrine therapy, many patients have primary resistance or develop resistance to endocrine therapies. Acquired resistance to endocrine therapy is a great challenge in the treatment of ER+ breast cancer patient. Here we showed that Response Gene to Complement (RGC)-32 expression is higher in breast cancer than paired normal tissues, which was a poor predictive factor. RGC-32 overexpression resulted in tamoxifen resistance, whereas knockdown of RGC-32 in tamoxifen-resistant cells restored tamoxifen sensitivity. Tamoxifen resistance mediated by RGC-32 was shown to be partially dependent on FoxM1 expression. Mechanistically, RGC-32 could activated PI3K signaling pathway, and then enhanced estrogen receptor alpha (ERα) activity. ERα activation is essential for RGC-32-mediated the expression of FoxM1. These data support that targeting RGC-32 could effectively mitigate cancer progression and tamoxifen resistance, offering a complementary therapeutic approach to reduce acquired endocrine resistance.
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