ArticleCell communication and signaling : CCS2026
Caspase-2 inhibits mitochondrial respiration in colorectal adenocarcinoma cells.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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