Scholarlink

<p>Bisphenol A (BPA), a synthetic endocrine-disrupting chemical, has been implicated in several diseases, including cancer. However, its effects on mitochondrial function in cervical cancer (CC) remain poorly understood. We investigated the effects of BPA on mitochondrial structure and function in SiHa and CaSki CC cell lines. Confocal microscopy revealed that BPA (1&#xa0;nM–1&#xa0;µM) disrupted mitochondrial morphology, increased circularity (<sup>*</sup><i>p</i> &lt; 0.05), and reduced branch length and content. BPA increased mitochondrial ROS (mtROS) and Ca<sup>2</sup>⁺ levels, decreased mitochondrial membrane potential (MMP) and mitochondrial mass, induced mtDNA depletion, and impaired oxidative respiration (OCR). Notably, BPA increased glucose uptake and lipid peroxidation while reducing the antioxidant (GSH and CAT) activity. A dose-dependent increase in mitochondrial lipid droplets (<i>p</i> &lt; 0.001) was accompanied by opposite ATP trends: ATP levels increased in SiHa cells but decreased in CaSki cells. Western blot and qRT‒PCR revealed the cell type–specific regulation of PGC1α, TFAM, and DRP1. Molecular docking revealed strong binding of BPA to IDH2 (docking score − 7.38), MAOB (− 6.29), and HK2 (− 3.208), which was further validated by stable MD simulation. Thus, BPA may induce mitochondrial dysfunction, metabolic changes, and oxidative stress in CC cells in vitro, suggesting a potential role in cervical carcinogenesis that warrants further in vivo investigation.</p> Graphical abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Bisphenol A disrupts mitochondrial homeostasis and promotes metabolic alterations in cervical cancer cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月30日

查看全文
  • Nadeem Ghani Khan,
  • Divya Adiga,
  • Kannath U. Sanjay,
  • Padmalatha Satwadi Rai,
  • Shama Prasada Kabekkodu

摘要

Bisphenol A (BPA), a synthetic endocrine-disrupting chemical, has been implicated in several diseases, including cancer. However, its effects on mitochondrial function in cervical cancer (CC) remain poorly understood. We investigated the effects of BPA on mitochondrial structure and function in SiHa and CaSki CC cell lines. Confocal microscopy revealed that BPA (1 nM–1 µM) disrupted mitochondrial morphology, increased circularity (*p < 0.05), and reduced branch length and content. BPA increased mitochondrial ROS (mtROS) and Ca2⁺ levels, decreased mitochondrial membrane potential (MMP) and mitochondrial mass, induced mtDNA depletion, and impaired oxidative respiration (OCR). Notably, BPA increased glucose uptake and lipid peroxidation while reducing the antioxidant (GSH and CAT) activity. A dose-dependent increase in mitochondrial lipid droplets (p < 0.001) was accompanied by opposite ATP trends: ATP levels increased in SiHa cells but decreased in CaSki cells. Western blot and qRT‒PCR revealed the cell type–specific regulation of PGC1α, TFAM, and DRP1. Molecular docking revealed strong binding of BPA to IDH2 (docking score − 7.38), MAOB (− 6.29), and HK2 (− 3.208), which was further validated by stable MD simulation. Thus, BPA may induce mitochondrial dysfunction, metabolic changes, and oxidative stress in CC cells in vitro, suggesting a potential role in cervical carcinogenesis that warrants further in vivo investigation.

Graphical abstract