Cancer-related Molecular Pathways
Peer reviewed
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The molecular functions of the CDK9/positive transcription elongation factor b (P-TEFb) axis, its role in super-enhancer-driven oncogenic programs, and the mechanisms by which CDK9 inhibition promotes apoptosis, epigenetic derepression, and tumor microenvironment remodeling are summarized.
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BACKGROUND: Cyclin-dependent kinase 9 (CDK9) is a central regulator of RNA polymerase II elongation and has emerged as a therapeutic target in tumors characterized by transcriptional addiction. Growing interest in selective inhibitors and targeted degraders has renewed attention to the translational potential of CDK9-directed therapy. AREAS COVERED: This review summarizes the molecular functions of the CDK9/positive transcription elongation factor b (P-TEFb) axis, its role in super-enhancer-driven oncogenic programs, and the mechanisms by which CDK9 inhibition promotes apoptosis, epigenetic derepression, and tumor microenvironment remodeling. We also discuss representative small-molecule inhibitors and proteolysis-targeting chimera (PROTAC) degraders, emerging biomarkers for patient stratification, rational combination strategies, and the current landscape of resistance mechanisms. EXPERT OPINION: Selective targeting of CDK9 offers a promising route for treating refractory malignancies, particularly when guided by transcriptional dependency, biomarker-informed dosing, and rational combination design. Future progress will likely depend on improving therapeutic index, refining translational biomarkers, and anticipating adaptive resistance during clinical development.
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@article{Liu2026Molecular,
title = {Molecular targeting of CDK9 in oncology therapeutics: avenues for translational impact},
author = {Tiyao Liu and Zhongran Liu and Wenjing Wei and Shudong Wang and Shaoqiang Wang and Yuanyuan Zhang and Ziyi Gao and Wenhao Wu},
journal = {Expert Opinion on Therapeutic Targets},
year = {2026},
doi = {10.1080/14728222.2026.2723483},
url = {https://doi.org/10.1080/14728222.2026.2723483}
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