细胞周期蛋白依赖性激酶 9 (CDK9) 通过促进 RNA Pol II 延伸来调节 mRNA 转录。 CDK9 现在正成为癌症的潜在治疗靶点，因为已发现其过度表达与癌症发展和较差的临床结果相关。虽然 CDK9 抑制方面的许多工作都集中在血液恶性肿瘤上，但这种癌症驱动因素在实体瘤中的作用开始成为人们关注的焦点。许多实体癌也过度表达 CDK9，并依赖其活性来促进下游致癌信号通路。本文综述了实体瘤中CDK9生物学的最新知识以及小分子CDK9抑制剂的研究。我们讨论 CDK9 抑制剂在实体瘤中的最新临床试验结果，重点关注提高此类药物治疗效果需要考虑的关键问题。版权所有 © 2024 Elsevier Inc. 保留所有权利。

Cyclin-dependent kinase 9 (CDK9) regulates mRNA transcription by promoting RNA Pol II elongation. CDK9 is now emerging as a potential therapeutic target for cancer, since its overexpression has been found to correlate with cancer development and worse clinical outcomes. While much work on CDK9 inhibition has focused on hematologic malignancies, the role of this cancer driver in solid tumors is starting to come into focus. Many solid cancers also overexpress CDK9 and depend on its activity to promote downstream oncogenic signaling pathways. In this review, we summarize the latest knowledge of CDK9 biology in solid tumors and the studies of small molecule CDK9 inhibitors. We discuss the results of the latest clinical trials of CDK9 inhibitors in solid tumors, with a focus on key issues to consider for improving the therapeutic impact of this drug class.Copyright © 2024 Elsevier Inc. All rights reserved.