ArticleAnnals of translational medicine2021
Caseinolytic protease P (CLPP) activated by ONC201 inhibits proliferation and promotes apoptosis in human epithelial ovarian cancer cells by inducing mitochondrial dysfunction.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- ONC201/dordaviprone for H3 K27M-mutant tumors: Discovery, mechanisms, therapeutic potential, and future directions.Genes & diseases · 2027Review
- Mitochondrial Protease ClpP: Cancer Marker and Drug Target.Pharmaceuticals (Basel, Switzerland) · 2025Review
- A bird's eye view of mitochondrial unfolded protein response in cancer: mechanisms, progression and further applications.Cell death & disease · 2024Review
- ONC206 targeting ClpP induces mitochondrial dysfunction and protective autophagy in hepatocellular carcinoma cells.Neoplasia (New York, N.Y.) · 2024Article
- The mitochondrial protease ClpP is a druggable target that controls VSMC phenotype by a SIRT1-dependent mechanism.Redox biology · 2024Article
- A novel mitochondria-related core gene signature to predict the prognosis and evaluate tumour microenvironment in CESC single-cell validation.Journal of cellular and molecular medicine · 2024Article
- HSPA8-mediated stability of the CLPP protein regulates mitochondrial autophagy in cisplatin-resistant ovarian cancer cells.Acta biochimica et biophysica Sinica · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCaseinolytic protease P (CLPP) is a mitochondrial specific protein which has been reported to be related to tumor cell apoptosis. This study aims to explore the roles of CLPP in human epithelial ovarian cancer (EOC).
methodsWe determined CLPP expression in paracancerous tissues and cancer tissues obtained from 20 EOC patients, and also in 4 EOC cell lines, and one normal ovarian cell line (IOSE-80). We knocked CLPP expression down in SK-OV-3 and A2780 cells and overexpressed it in SW626 and OVcar3 cells. The effect of CLPP expression on cell proliferation, mitochondrial membrane potential, and apoptosis was then assessed by flow cytometry assay. Furthermore, the effect of ONC201 (agonist of CLPP) on the EOC cell lines was also investigated.
resultsThe CLPP expression was markedly down-regulated in EOC cancer tissues, and the Kaplan-Meier Plotter database revealed its low expression was linked to poor prognosis in EOC patients. Low expression of CLPP up-regulated the expression of NADH: ubiquinone oxidoreductase subunit A12 (NDUFA12), succinate dehydrogenase complex flavoprotein subunit A (SDHA), and succinate dehydrogenase complex iron sulfur subunit B (SDHB), which are key members of the mitochondrial respiratory chain, and these up-regulated proteins further led to the increase of mitochondrial membrane potential, cell proliferation promotion and neoplasm metastasis. Conversely, while overexpression of CLPP led to the opposite results, including inducing the decrease of mitochondrial membrane potential and apoptosis. In addition, stimulation with ONC201 enhanced the function of CLPP in SW626 and OVcar3 cells, and silencing of CLPP could neutralize the effect of ONC201.
conclusionsOur findings suggest that CLPP mediated mitochondrial dysfunction inhibits the proliferation and migration of EOC cells.
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