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<p>High-risk human papillomavirus (HPV) oncoproteins E6/E7 are essential for cellular carcinogenesis and malignant growth in HPV-positive cervical cancers, and these oncoproteins have been considered as promising targets for cervical cancer treatment. Here, for the first time, we report that piericidin F (PdF), a new piericidin derivative derived from marine <i>Streptomyces</i>, inhibits cell proliferation and induces cell apoptosis in HPV-positive human cervical cancer HeLa cells. Molecular mechanism studies showed that PdF disrupted the mitochondria function and inhibited the function of mitochondrial respiration chains complex I. Subsequently, this increased generation of ROS stimulates oncoproteins E6/E7 degradation <i>via</i> ubiquitin proteasome system. In short, we reveal a new mechanism underlying the anti-cancer activity of piericidin compounds by disrupting mitochondrial function and degrading oncoproteins E6/E7 in HPV-positive cervical cancers, and highlight that PdF has the potential to be a lead compound for therapeutic agents against HPV-positive cervical cancers.</p>

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Piericidin F, a Novel Marine-Derived Piericidin Derivative, Degrades High-Risk HPV Oncoproteins E6/E7 by ROS-Dependent Ubiquitin Proteasome System and Induces Apoptosis in HeLa Cells

  • 期刊论文

  • 发表日期：

    2026年5月13日

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  • Weiyi Zhang,
  • Yifan Chen,
  • Yimin Chang,
  • Xiaoning Han,
  • Yufeng Yang,
  • Qianqun Gu,
  • Dehai Li,
  • Ming Liu

摘要

High-risk human papillomavirus (HPV) oncoproteins E6/E7 are essential for cellular carcinogenesis and malignant growth in HPV-positive cervical cancers, and these oncoproteins have been considered as promising targets for cervical cancer treatment. Here, for the first time, we report that piericidin F (PdF), a new piericidin derivative derived from marine Streptomyces, inhibits cell proliferation and induces cell apoptosis in HPV-positive human cervical cancer HeLa cells. Molecular mechanism studies showed that PdF disrupted the mitochondria function and inhibited the function of mitochondrial respiration chains complex I. Subsequently, this increased generation of ROS stimulates oncoproteins E6/E7 degradation via ubiquitin proteasome system. In short, we reveal a new mechanism underlying the anti-cancer activity of piericidin compounds by disrupting mitochondrial function and degrading oncoproteins E6/E7 in HPV-positive cervical cancers, and highlight that PdF has the potential to be a lead compound for therapeutic agents against HPV-positive cervical cancers.