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靶向JWA用于癌症治疗:功能、机制与药物研发

Targeting JWA for Cancer Therapy: Functions, Mechanisms and Drug Discovery.

作者信息

Ding Kun, Liu Xia, Wang Luman, Zou Lu, Jiang Xuqian, Li Aiping, Zhou Jianwei

机构信息

Department of Molecular Cell Biology & Toxicology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China.

Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 211166, China.

出版信息

Cancers (Basel). 2022 Sep 24;14(19):4655. doi: 10.3390/cancers14194655.

DOI:10.3390/cancers14194655
PMID:36230577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9564207/
Abstract

Tumor heterogeneity limits the precision treatment of targeted drugs. It is important to find new tumor targets. JWA, also known as ADP ribosylation factor-like GTPase 6 interacting protein 5 (ARL6IP5, GenBank: AF070523, 1998), is a microtubule-associated protein and an environmental response gene. Substantial evidence shows that JWA is low expressed in a variety of malignancies and is correlated with overall survival. As a tumor suppressor, JWA inhibits tumor progression by suppressing multiple oncogenes or activating tumor suppressor genes. Low levels of JWA expression in tumors have been reported to be associated with multiple aspects of cancer progression, including angiogenesis, proliferation, apoptosis, metastasis, and chemotherapy resistance. In this review, we will discuss the structure and biological functions of JWA in tumors, examine the potential therapeutic strategies for targeting JWA and explore the directions for future investigation.

摘要

肿瘤异质性限制了靶向药物的精准治疗。寻找新的肿瘤靶点很重要。JWA,也称为ADP核糖基化因子样GTP酶6相互作用蛋白5(ARL6IP5,基因库:AF070523,1998),是一种微管相关蛋白和环境反应基因。大量证据表明,JWA在多种恶性肿瘤中低表达,且与总生存期相关。作为一种肿瘤抑制因子,JWA通过抑制多个癌基因或激活肿瘤抑制基因来抑制肿瘤进展。据报道,肿瘤中JWA表达水平低与癌症进展的多个方面相关,包括血管生成、增殖、凋亡、转移和化疗耐药性。在本综述中,我们将讨论JWA在肿瘤中的结构和生物学功能,研究靶向JWA的潜在治疗策略,并探索未来的研究方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/2470f9b3c65b/cancers-14-04655-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/faa31be4295c/cancers-14-04655-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/62004dc5dfc5/cancers-14-04655-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/edd272fec372/cancers-14-04655-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/2470f9b3c65b/cancers-14-04655-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/faa31be4295c/cancers-14-04655-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/62004dc5dfc5/cancers-14-04655-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/edd272fec372/cancers-14-04655-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9eab/9564207/2470f9b3c65b/cancers-14-04655-g004.jpg

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本文引用的文献

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Metastasis.转移。
Cancer Cell. 2022 Aug 8;40(8):787-791. doi: 10.1016/j.ccell.2022.07.010.
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JAC4 Protects from X-ray Radiation-Induced Intestinal Injury by JWA-Mediated Anti-Oxidation/Inflammation Signaling.JAC4通过JWA介导的抗氧化/炎症信号通路保护免受X射线辐射诱导的肠道损伤。
Antioxidants (Basel). 2022 May 27;11(6):1067. doi: 10.3390/antiox11061067.
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Resistance mechanisms to HER2-targeted therapy in gastroesophageal adenocarcinoma: A systematic review.胃食管腺癌中针对 HER2 靶向治疗的耐药机制:系统评价。
Cancer Treat Rev. 2022 Jul;108:102418. doi: 10.1016/j.ctrv.2022.102418. Epub 2022 May 30.
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Lymph node colonization induces tumor-immune tolerance to promote distant metastasis.淋巴结定植诱导肿瘤免疫耐受以促进远处转移。
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Targeting mutations in cancer.靶向癌症中的突变
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IFNα Potentiates Anti-PD-1 Efficacy by Remodeling Glucose Metabolism in the Hepatocellular Carcinoma Microenvironment.IFNα 通过重塑肝癌微环境中的葡萄糖代谢增强抗 PD-1 疗效。
Cancer Discov. 2022 Jul 6;12(7):1718-1741. doi: 10.1158/2159-8290.CD-21-1022.
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JAC1 targets YY1 mediated JWA/p38 MAPK signaling to inhibit proliferation and induce apoptosis in TNBC.JAC1靶向YY1介导的JWA/p38丝裂原活化蛋白激酶信号通路,以抑制三阴性乳腺癌的增殖并诱导其凋亡。
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