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miRNA/AKT3 调控轴在人类癌症中的多功能性。

The Multifunctional Nature of the MicroRNA/AKT3 Regulatory Axis in Human Cancers.

机构信息

Research Center of CHU Sainte-Justine, University of Montréal, Montreal, QC H3T 1C5, Canada.

Department of Pharmacology and Physiology, Department of Pediatrics, University of Montréal, Montreal, QC H3T 1C5, Canada.

出版信息

Cells. 2023 Nov 9;12(22):2594. doi: 10.3390/cells12222594.

DOI:10.3390/cells12222594
PMID:37998329
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10670075/
Abstract

Serine/threonine kinase (AKT) signaling regulates diverse cellular processes and is one of the most important aberrant cell survival mechanisms associated with tumorigenesis, metastasis, and chemoresistance. Targeting AKT has become an effective therapeutic strategy for the treatment of many cancers. AKT3 (PKBγ), the least studied isoform of the AKT family, has emerged as a major contributor to malignancy. AKT3 is frequently overexpressed in human cancers, and many regulatory oncogenic or tumor suppressor small non-coding RNAs (ncRNAs), including microRNAs (miRNAs), have recently been identified to be involved in regulating AKT3 expression. Therefore, a better understanding of regulatory miRNA/AKT3 networks may reveal novel biomarkers for the diagnosis of patients with cancer and may provide invaluable information for developing more effective therapeutic strategies. The aim of this review was to summarize current research progress in the isoform-specific functions of AKT3 in human cancers and the roles of dysregulated miRNA/AKT3 in specific types of human cancers.

摘要

丝氨酸/苏氨酸激酶(AKT)信号通路调节多种细胞过程,是与肿瘤发生、转移和化疗耐药性相关的最重要的异常细胞存活机制之一。针对 AKT 已成为治疗许多癌症的有效治疗策略。AKT3(PKBγ)是 AKT 家族中研究最少的同工型,已成为恶性肿瘤的主要贡献者。AKT3 在人类癌症中经常过表达,并且许多调节致癌或肿瘤抑制性小非编码 RNA(ncRNA),包括 microRNAs(miRNAs),最近被确定参与调节 AKT3 的表达。因此,更好地理解调节 miRNA/AKT3 网络可能为癌症患者的诊断提供新的生物标志物,并为开发更有效的治疗策略提供宝贵的信息。本综述的目的是总结 AKT3 在人类癌症中的同工型特异性功能的最新研究进展,以及失调的 miRNA/AKT3 在特定类型的人类癌症中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/2319894a7539/cells-12-02594-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/c9406c734eac/cells-12-02594-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/98686ab8beaf/cells-12-02594-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/2319894a7539/cells-12-02594-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/c9406c734eac/cells-12-02594-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/98686ab8beaf/cells-12-02594-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ab/10670075/2319894a7539/cells-12-02594-g003.jpg

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