ArticleDiscover oncology2026
CDK9 inhibitor A09-003 overcomes TRAIL resistance via dual Mcl-1 suppression in breast cancer cells.
Article in Discover oncology, 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
backgroundResistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a main limitation in breast cancer therapy. Identifying effective sensitizers is crucial to overcome this hurdle. Cyclin-dependent kinase-9 (CDK-9) inhibition has recently emerged as a potential strategy to enhance apoptotic responses in cancer cells. MATERIALS AND
methodsWe investigated the effect of A09-003, a novel CDK9 inhibitor, on TRAIL-induced apoptosis and cell signaling in TNBC breast cancer cells. Cell viability was assessed by CellTiter-Glo assays, while apoptotic induction was evaluated using Flow cytometry analysis with Annexin V/PI staining, DNA fragmentation, and caspase activity assay. Protein expression levels of Mcl-1 and death receptors were analyzed via Western blotting and real time PCR. Mechanistic studies explored Mcl-1 protein degradation and transcriptional regulation through CDK-9 inhibition.
resultsA09-003 significantly enhanced TRAIL-induced apoptosis in tested breast cancer cells by increasing death receptor 5 expression, promoting caspase activation, and DNA fragmentation. Mechanistically, A09-003 downregulated Mcl-1 expression through dual pathways: promoting its proteasomal degradation and suppressing transcription via inhibition of CDK9-dependent RNA polymerase II phosphorylation.
conclusionA09-003 restores TRAIL sensitivity through Mcl-1 downregulation, identifying CDK-9 as a therapeutic target in resistant breast cancers.
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