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细胞周期检查点的变革:对抗恶性肿瘤的靶向治疗

Cell cycle checkpoint revolution: targeted therapies in the fight against malignant tumors.

作者信息

Song Guangming, Liu Jue, Tang Xing, Zhong Jie, Zeng Yuhuan, Zhang Xiaodi, Zhou Jianbin, Zhou Jie, Cao Lu, Zhang Qunfeng, Li Yukun

机构信息

Department of Obstetrics and Gynecology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Department of Assisted Reproductive Centre, The affiliated Zhuzhou hospital Xiangya medical college, Central South University, Zhuzhou, Hunan, China.

出版信息

Front Pharmacol. 2024 Oct 11;15:1459057. doi: 10.3389/fphar.2024.1459057. eCollection 2024.

DOI:10.3389/fphar.2024.1459057
PMID:39464635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11505109/
Abstract

Malignant tumors are among the most important causes of death worldwide. The pathogenesis of a malignant tumor is complex and has not been fully elucidated. Studies have shown that such pathogenesis is related to abnormal cell cycle progression. The expression levels of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors as well as functions of the cell cycle checkpoints determine whether the cell cycle progression is smooth. Cell-cycle-targeting drugs have the advantages of high specificity, low toxicity, low side effects, and low drug resistance. Identifying drugs that target the cell cycle and applying them in clinical treatments are expected to promote chemotherapeutic developments against malignant tumors. This article aims to review drugs targeted against the cell cycle and their action mechanisms.

摘要

恶性肿瘤是全球最重要的死亡原因之一。恶性肿瘤的发病机制复杂,尚未完全阐明。研究表明,这种发病机制与细胞周期进程异常有关。细胞周期蛋白、细胞周期蛋白依赖性激酶(CDK)和CDK抑制剂的表达水平以及细胞周期检查点的功能决定了细胞周期进程是否顺利。靶向细胞周期的药物具有特异性高、毒性低、副作用小和耐药性低等优点。识别靶向细胞周期的药物并将其应用于临床治疗有望推动恶性肿瘤化疗的发展。本文旨在综述靶向细胞周期的药物及其作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/11505109/cbc5932a8956/fphar-15-1459057-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/11505109/96c6f9810ab5/fphar-15-1459057-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/11505109/cbc5932a8956/fphar-15-1459057-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/11505109/96c6f9810ab5/fphar-15-1459057-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/11505109/cbc5932a8956/fphar-15-1459057-g002.jpg

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本文引用的文献

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ESM1 enhances fatty acid synthesis and vascular mimicry in ovarian cancer by utilizing the PKM2-dependent warburg effect within the hypoxic tumor microenvironment.ESM1 通过在缺氧肿瘤微环境中利用 PKM2 依赖性瓦博格效应增强脂肪酸合成和血管拟态在卵巢癌中的作用。
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YY2/BUB3 Axis promotes SAC Hyperactivation and Inhibits Colorectal Cancer Progression via Regulating Chromosomal Instability.
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YTHDF1/RNF7/p27 axis promotes prostate cancer progression.YTHDF1/RNF7/p27轴促进前列腺癌进展。
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Harnessing bacterial metabolites for enhanced cancer chemotherapy: unveiling unique therapeutic potentials.利用细菌代谢物增强癌症化疗:揭示独特的治疗潜力。
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YY2/BUB3 轴通过调节染色体不稳定性促进 SAC 过度激活并抑制结直肠癌进展。
Adv Sci (Weinh). 2024 Jul;11(26):e2308690. doi: 10.1002/advs.202308690. Epub 2024 Apr 29.
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Inhibition of CDK1 by RO-3306 Exhibits Anti-Tumorigenic Effects in Ovarian Cancer Cells and a Transgenic Mouse Model of Ovarian Cancer.RO-3306 通过抑制 CDK1 在卵巢癌细胞和卵巢癌转基因小鼠模型中表现出抗肿瘤作用。
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