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探讨黑色素瘤中的 STK3:信号网络及治疗机会的系统综述。

Exploring STK3 in melanoma: a systematic review of signaling networks and therapeutic opportunities.

机构信息

Department of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.

Department of Clinical Pharmacy, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran.

出版信息

Mol Biol Rep. 2024 Nov 22;52(1):8. doi: 10.1007/s11033-024-10064-z.

DOI:10.1007/s11033-024-10064-z
PMID:39576434
Abstract

Melanoma is an aggressive cancer that disregards both the MAPK and Hippo signaling pathways. This systematic review explores STK3 function in the Hippo pathway to regulate networks and its therapeutic potential in melanoma. From 1991 to 2024, we studied how STK3 interacts with the MAPK/ERK pathway to promote apoptosis and inhibit tumor growth. STK3 controls cell growth, apoptosis, and metastasis via the Hippo and MAPK pathways. It is a melanoma tumor suppressor. Some ways to target STK3 are to directly activate it, stop downstream effectors like YAP/TAZ from working, or use existing BRAF inhibitors together with other methods. Despite advancements, challenges in STK3 drug development persist, warranting further investigation. This review examined the role of STK3 in the development of melanoma and identified potential vulnerabilities for therapeutic intervention.

摘要

黑色素瘤是一种侵袭性癌症,它无视 MAPK 和 Hippo 信号通路。本系统综述探讨了 STK3 在 Hippo 通路中的功能,以调节网络及其在黑色素瘤中的治疗潜力。从 1991 年到 2024 年,我们研究了 STK3 如何与 MAPK/ERK 通路相互作用以促进细胞凋亡并抑制肿瘤生长。STK3 通过 Hippo 和 MAPK 通路控制细胞生长、凋亡和转移。它是一种黑色素瘤肿瘤抑制因子。靶向 STK3 的一些方法是直接激活它,阻止下游效应物如 YAP/TAZ 发挥作用,或与其他方法一起使用现有的 BRAF 抑制剂。尽管取得了进展,但 STK3 药物开发仍然存在挑战,需要进一步研究。本综述检查了 STK3 在黑色素瘤发展中的作用,并确定了治疗干预的潜在脆弱性。

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Theranostics. 2024 Jan 1;14(2):593-607. doi: 10.7150/thno.85437. eCollection 2024.
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Inhibition of TAZ impairs the migration ability of melanoma cells.TAZ的抑制作用会损害黑色素瘤细胞的迁移能力。
Open Life Sci. 2023 Jun 21;18(1):20220633. doi: 10.1515/biol-2022-0633. eCollection 2023.
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Serine/threonine kinase 3 promotes oxidative stress and mitochondrial damage in septic cardiomyopathy through inducing Kelch-like ECH-associated protein 1 phosphorylation and nuclear factor erythroid 2-related factor 2 degradation.
丝氨酸/苏氨酸激酶 3 通过诱导 Kelch 样 ECH 相关蛋白 1 磷酸化和核因子红细胞 2 相关因子 2 降解促进脓毒症性心肌病中的氧化应激和线粒体损伤。
Int J Biol Sci. 2023 Feb 21;19(5):1369-1381. doi: 10.7150/ijbs.80800. eCollection 2023.
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WNT5a Signaling through ROR2 Activates the Hippo Pathway to Suppress YAP1 Activity and Tumor Growth.WNT5a 通过 ROR2 信号激活 Hippo 通路,抑制 YAP1 活性并抑制肿瘤生长。
Cancer Res. 2023 Apr 4;83(7):1016-1030. doi: 10.1158/0008-5472.CAN-22-3003.
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