ArticleCellular and molecular life sciences : CMLS2026
CircRPPH1 promotes hepatocellular carcinoma progression through inhibiting PPARα transcription and accelerating its ubiquitination and degradation.
Article in Cellular and molecular life sciences : CMLS, 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
backgroundHepatocellular carcinoma (HCC) is a prominent cause of cancer-related mortality globally. It is urgently necessary to elucidate the pathogenesis of HCC and develop novel therapeutic strategies. Although certain circular RNAs (circRNAs) act as oncogenic drivers in HCC progression, the underlying mechanisms remain poorly understood.
methodsCircRNA-miRNA-mRNA network was established to screen potential circRNAs that were associated with HCC progression. CCK8, colony formation, EdU staining, wound healing, transwell assay and xenograft models were implemented to investigate the role of circRPPH1 in HCC progression. RNA-seq, luciferase reporter assays, Turbo-ID, mass spectrometry, co-immunoprecipitation and RNA-binding protein immunoprecipitation assays and rescue experiments were employed to determine the underlying molecular mechanism.
resultsCircRPPH1 was significantly upregulated in HCC tissues and it promoted HCC progression both in vitro and in vivo. The elevated circRPPH1 expression in HCC was due to its increased stability, which was mediated by m
conclusionsCircRPPH1 is a tumor-promoting circRNA, which inhibits PPARα transcription through miR-7845-5p/SOX4 axis and accelerates its ubiquitination and degradation through competitively binding with USP1. These findings suggest that circRPPH1 may serve as a promising therapeutic target for HCC treatment.
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