ArticleGenes & genomics2026
CDK9 inhibition triggers MT2A-dependent apoptosis in HCC cells.
Article in Genes & genomics, 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 leading cause of cancer-related mortality worldwide. While cyclin-dependent kinase 9 (CDK9) is recognized as a crucial transcriptional regulator in cancer progression, its specific role in HCC pathogenesis remains poorly understood.
objectiveThis study aims to investigate the specific role and underlying mechanisms of cyclin-dependent kinase 9 (CDK9) in the pathogenesis and progression of hepatocellular carcinoma (HCC).
methodsCDK9 expression in HCC was analyzed through public databases and validated by immunohistochemistry (IHC) of clinical specimens. Compound 45 (CDK9 inhibitor) was used to assess CDK9’s functional impact. Mechanistic studies employed RNA sequencing (RNA-seq), chromatin immunoprecipitation (ChIP), immunoblotting, RT-qPCR, flow cytometry, and colony formation assays. Antitumor efficacy was evaluated in xenograft models.
resultsOur study demonstrates significant CDK9 overexpression in HCC clinical samples, as confirmed through the cBioPortal for Cancer Genomics database analysis and IHC validation, with elevated expression correlating strongly with poor patient prognosis. Importantly, we reveal that pharmacological inhibition of CDK9 using Compound 45 potently induces apoptosis in HCC cells through a novel molecular mechanism. Mechanistic investigations show that CDK9 inhibition promotes c-Jun-mediated transcriptional activation of MT2A, leading to subsequent downregulation of the anti-apoptotic proteins BCL-2 and BCL-XL. Genetic ablation experiments confirm the essential role of MT2A in mediating this apoptotic pathway. Furthermore, in vivo studies using an HCC xenograft model demonstrate the significant tumor-suppressive effects of Compound 45 treatment.
conclusionThese findings collectively identify the CDK9/c-Jun/MT2A/BCL-2/BCL-XL axis as a critical therapeutic pathway in HCC, establishing CDK9 inhibition as a promising strategy for HCC treatment.
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