Suppr超能文献

揭示 MYH9 在肿瘤生物学中神秘角色:全面综述。

Unveiling the enigmatic role of MYH9 in tumor biology: a comprehensive review.

机构信息

Department of Urology Il, The First Hospital of Jilin University, Changchun, 130021, China.

Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, 130021, China.

出版信息

Cell Commun Signal. 2024 Aug 27;22(1):417. doi: 10.1186/s12964-024-01781-w.

Abstract

Non-muscle myosin heavy chain IIA (MYH9), a member of the non-muscle myosin II (NM II) family, is widely expressed in cells. The interaction of MYH9 with actin in the cytoplasm can hydrolyze ATP, completing the conversion of chemical energy to mechanical motion. MYH9 participates in various cellular processes, such as cell adhesion, migration, movement, and even signal transduction. Mutations in MYH9 are often associated with autosomal dominant platelet disorders and kidney diseases. Over the past decade, tumor-related research has gradually revealed a close relationship between MYH9 and the occurrence and development of tumors. This article provides a review of the research progress on the role of MYH9 in cancer regulation. We also discussed the anti-cancer effects of MYH9 under special circumstances, as well as its regulation of T cell function. In addition, given the importance of MYH9 as a key hub in oncogenic signal transduction, we summarize the current therapeutic strategies targeting MYH9 as well as the ongoing challenges.

摘要

非肌肉肌球蛋白重链 IIA(MYH9)是一种广泛存在于细胞中的非肌肉肌球蛋白 II(NM II)家族成员。MYH9 与细胞质中的肌动蛋白相互作用可以水解 ATP,完成化学能量向机械运动的转化。MYH9 参与多种细胞过程,如细胞黏附、迁移、运动,甚至信号转导。MYH9 的突变常与常染色体显性血小板疾病和肾脏疾病有关。在过去的十年中,肿瘤相关研究逐渐揭示了 MYH9 与肿瘤发生和发展之间的密切关系。本文综述了 MYH9 在癌症调控中的作用的研究进展。我们还讨论了 MYH9 在特殊情况下的抗癌作用及其对 T 细胞功能的调节。此外,鉴于 MYH9 作为致癌信号转导关键枢纽的重要性,我们总结了目前针对 MYH9 的治疗策略以及正在面临的挑战。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ff9/11351104/3d5a2d2a7a40/12964_2024_1781_Fig2_HTML.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验