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Response Gene to Complement 32 promotes cell proliferation and tamoxifen resistance in breast cancer via elevated

Xinlei Li1, Yan Liu2, Zhiqian Wang3

  • 1Medical College of Qingdao University, Qingdao, China.

Plos One
|July 28, 2025
PubMed

Insights

Response Gene to Complement (RGC)-32 is elevated in breast cancer, driving tamoxifen resistance by activating PI3K/ERα signaling and FoxM1. Targeting RGC-32 may overcome endocrine resistance in ER+ breast cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Estrogen receptor-positive (ER+) breast cancer often develops resistance to endocrine therapy, a significant clinical challenge.
  • Acquired resistance limits the long-term efficacy of treatments like tamoxifen.

Purpose of the Study:

  • To investigate the role of Response Gene to Complement (RGC)-32 in endocrine resistance in ER+ breast cancer.
  • To elucidate the molecular mechanisms underlying RGC-32-mediated tamoxifen resistance.

Main Methods:

  • Quantitative analysis of RGC-32 expression in breast cancer tissues.
  • In vitro studies involving RGC-32 overexpression and knockdown in breast cancer cell lines.
  • Assessment of tamoxifen sensitivity, PI3K/ERα signaling, and FoxM1 expression.

Main Results:

  • RGC-32 expression is upregulated in breast cancer and correlates with poor prognosis.
  • RGC-32 overexpression induces tamoxifen resistance; its knockdown restores sensitivity.
  • RGC-32 activates the PI3K pathway, enhancing estrogen receptor alpha (ERα) activity, which is crucial for FoxM1 expression.

Conclusions:

  • RGC-32 is a key mediator of tamoxifen resistance in ER+ breast cancer.
  • Targeting RGC-32 presents a potential strategy to overcome acquired endocrine resistance.
  • RGC-32 inhibition could offer a complementary therapeutic approach for managing resistant breast cancer.

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