ArticleInternational journal of molecular medicine2025
CDC5L binds to ELAVL1 to inhibit pyroptosis in hepatocellular carcinoma through the Caspase 3/GSDME signaling pathway.
Article in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
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7 authors.
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Abstract
Hepatocellular carcinoma (HCC) is associated with elevated rates of illness and mortality, posing a significant challenge to global health. Elevated levels of cell division cycle 5 like (CDC5L) in HCC predict a poor prognosis. The present study aimed to elucidate the role of CDC5L in HCC. First, CDC5L expression was detected using bioinformatics analysis and validated on clinical samples and cells. Next, CDC5L was knocked down and overexpressed. CDC5L and Caspase 3 knockdown was conducted to explore the effect on pyroptosis in HCC. The mechanisms of HCC pyroptosis were investigated by interfering with and overexpressing ELAV like RNA binding protein 1 (ELAVL1), as well as interfering with CDC5L and overexpressing ELAVL1. Finally, the role of CDC5L/ELAVL1 in regulating Caspase 3/Caspase 3‑-gasdermin E (GSDME) in HCC pyroptosis was validated through cellular and animal experiments. It was found that CDC5L expression was increased in HCC. Elevated CDC5L levels were linked to adverse outcomes in HCC. Suppressing CDC5L expression reduced cell viability, curbed cell proliferation and diminished cell migration and invasion capabilities, while simultaneously enhancing pyroptosis. Additionally, CDC5L knockdown resulted in a progressive decline in tumor volume and a decrease in tumor size and weight. CDC5L overexpression exerted an opposite effect. Moreover, regulating pyroptosis in HCC by CDC5L was dependent on Caspase family. Following CDC5L knockdown, tumor volume steadily diminished, tumor mass shrank and tumor weight was correspondingly reduced. ELAVL1 overexpression reversed these effects. CDC5L competitively bound to ELAVL1 to inhibit the binding of ELAVL1 with
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