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<p>Cyclophosphamide (CTX) is a primary medicine for curing breast cancer which often causes premature ovarian insufficiency (POI). Our recent publication reveals that CTX induces POI by promoting the expression of SLC1A4, a transporter of serine efflux, in ovarian granulosa cells (GCs). Here, we report that there is a closed connection between the reduction of serum serine and ovarian hypofunction in the breast cancer patients treated with CTX or women of childbearing age who are suffered from the staying-up-late. Additionally, we observe that dietary serine supplementation protects mice from CTX-induced POI without altering its anti-breast cancer. Furthermore, we demonstrate that the elevated serine promotes S1P synthesis, and in turn, inhibits the nuclear translocation of Nrf2 and consequent HO-1 expression, to suppress ferroptosis in GCs. Our study reveals that the chemotherapy-induced or idiopathic POI share the same mechanisms, indicating that serine is a critical factor for maintaining ovarian function.</p>

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Serine inhibits granulosa cell ferroptosis to maintain ovarian function

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月21日

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  • Hao-Cheng Gu,
  • You-Qiong Zhuo,
  • Ling-Fang Wang,
  • Yu-Wei Zhang,
  • Dong-Shui Li,
  • Ling-Qin Chen,
  • Zhi-Hua Li,
  • Yun-Yue Wang,
  • Yi-Kai Wang,
  • Hui-Ting Liao,
  • Jia-Qin Wu,
  • Shi-Qing Tao,
  • Xing-Yu Wei,
  • Ke-Yu Deng,
  • Hong-Bo Xin

摘要

Cyclophosphamide (CTX) is a primary medicine for curing breast cancer which often causes premature ovarian insufficiency (POI). Our recent publication reveals that CTX induces POI by promoting the expression of SLC1A4, a transporter of serine efflux, in ovarian granulosa cells (GCs). Here, we report that there is a closed connection between the reduction of serum serine and ovarian hypofunction in the breast cancer patients treated with CTX or women of childbearing age who are suffered from the staying-up-late. Additionally, we observe that dietary serine supplementation protects mice from CTX-induced POI without altering its anti-breast cancer. Furthermore, we demonstrate that the elevated serine promotes S1P synthesis, and in turn, inhibits the nuclear translocation of Nrf2 and consequent HO-1 expression, to suppress ferroptosis in GCs. Our study reveals that the chemotherapy-induced or idiopathic POI share the same mechanisms, indicating that serine is a critical factor for maintaining ovarian function.