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<p>Knockout of caspase-2 in colorectal adenocarcinoma cells enhances mitochondrial oxygen consumption supported by succinate, a substrate of complex II. Additionally, caspase-2 knockout stimulates oxidative stress and promotes cell proliferation. The restriction of oxygen consumption by caspase-2 was attributed to the suppression of transcription of succinate dehydrogenase subunit B (SDHB), translocase of the outer mitochondrial membrane (TOMM), and the translocase of the inner mitochondrial membrane (TIMM). Caspase-2 knockout also increased the expression of the transcription factors p53 and c-Jun, which regulate the expression of mitochondria-related genes. Importantly, the catalytic activity of caspase-2 was dispensable for controlling mitochondrial respiration. In caspase-2 knockout mice, SDHA content remained unchanged, while SDHB and TIMM23 levels tended to increase, with TOMM20 showing the most prominent upregulation. Collectively, our findings uncover a novel molecular signaling pathway regulated by caspase-2 that may contribute to tumor growth suppression.</p>

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Caspase-2 inhibits mitochondrial respiration in colorectal adenocarcinoma cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Chanin Sillapachaiyaporn,
  • Maria A. Yapryntseva,
  • Aygun R. Mamedova,
  • Lina Abdelghany,
  • Vladimir Gogvadze,
  • Boris Zhivotovsky

摘要

Knockout of caspase-2 in colorectal adenocarcinoma cells enhances mitochondrial oxygen consumption supported by succinate, a substrate of complex II. Additionally, caspase-2 knockout stimulates oxidative stress and promotes cell proliferation. The restriction of oxygen consumption by caspase-2 was attributed to the suppression of transcription of succinate dehydrogenase subunit B (SDHB), translocase of the outer mitochondrial membrane (TOMM), and the translocase of the inner mitochondrial membrane (TIMM). Caspase-2 knockout also increased the expression of the transcription factors p53 and c-Jun, which regulate the expression of mitochondria-related genes. Importantly, the catalytic activity of caspase-2 was dispensable for controlling mitochondrial respiration. In caspase-2 knockout mice, SDHA content remained unchanged, while SDHB and TIMM23 levels tended to increase, with TOMM20 showing the most prominent upregulation. Collectively, our findings uncover a novel molecular signaling pathway regulated by caspase-2 that may contribute to tumor growth suppression.