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<p>For patients with advanced endometrioid endometrial carcinoma (EEC), prognosis remains poor due to the lack of effective therapeutic targets. Loss of androgen receptor (AR) expression is associated with the progression of EEC. However, the regulatory mechanisms remain unknown, limiting its application in prognostic prediction and targeted therapy. In this study, overexpression of KLF12 or loss of AR was strongly correlated with advanced clinical stage and poor patient outcomes. Functional experiments demonstrated that KLF12 upregulation suppressed AR expression and promoted EEC metastasis by enhancing epithelial–mesenchymal transition (EMT) both in vitro and in vivo. As determined by bioinformatics predictions and CUT&amp;Tag analysis, KLF12 suppressed the transcriptional activity of the AR gene by binding to the promoter and intronic regions. These direct interactions were further confirmed through electrophoretic mobility shift assay (EMSA), ChIP-PCR, ChIP-qPCR and dual-luciferase reporter assays. This study identifies a novel KLF12–AR regulatory axis driving EEC metastasis and provides potential molecular targets for therapeutic intervention and prognostic evaluation.</p>

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KLF12-mediated suppression of androgen receptor accelerates metastasis in endometrioid endometrial carcinoma by activating epithelial–mesenchymal transition

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月23日

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  • Jian Li,
  • Ling Zhou,
  • Sihui Yang,
  • Yanping Zhu,
  • Haimeng Shi,
  • Feifei Guo,
  • Xiangyi Kong,
  • Lulu Wang,
  • Mengdan Miao,
  • Qi Guo,
  • Ruilin Chen,
  • Tong Yan,
  • Junnan Wang,
  • Qi Liu,
  • Ling Ding,
  • Huaijun Zhou

摘要

For patients with advanced endometrioid endometrial carcinoma (EEC), prognosis remains poor due to the lack of effective therapeutic targets. Loss of androgen receptor (AR) expression is associated with the progression of EEC. However, the regulatory mechanisms remain unknown, limiting its application in prognostic prediction and targeted therapy. In this study, overexpression of KLF12 or loss of AR was strongly correlated with advanced clinical stage and poor patient outcomes. Functional experiments demonstrated that KLF12 upregulation suppressed AR expression and promoted EEC metastasis by enhancing epithelial–mesenchymal transition (EMT) both in vitro and in vivo. As determined by bioinformatics predictions and CUT&Tag analysis, KLF12 suppressed the transcriptional activity of the AR gene by binding to the promoter and intronic regions. These direct interactions were further confirmed through electrophoretic mobility shift assay (EMSA), ChIP-PCR, ChIP-qPCR and dual-luciferase reporter assays. This study identifies a novel KLF12–AR regulatory axis driving EEC metastasis and provides potential molecular targets for therapeutic intervention and prognostic evaluation.