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P2嘌呤能受体在胃癌进展中的功能作用。

The functional role of P2 purinergic receptors in the progression of gastric cancer.

作者信息

Zou Fei-Long, Liu Ji-Peng, Zuo Cheng, He Peng-Fei, Ye Jin-Xiong, Zhang Wen-Jun

机构信息

Thyroid surgery, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen City, 518105, China.

The Second Affiliated Hospital, Nanchang University, Nanchang City, Jiangxi Province, 343000, China.

出版信息

Purinergic Signal. 2024 Mar 12. doi: 10.1007/s11302-024-10000-7.

DOI:10.1007/s11302-024-10000-7
PMID:38470513
Abstract

Studies have confirmed that P2 purinergic receptors (P2X receptors and P2Y receptors) expressed in gastric cancer (GC) cells and GC tissues and correlates with their function. Endogenous nucleotides including ATP, ADP, UTP, and UDP, as P2 purinergic receptors activators, participate in P2 purinergic signal transduction pathway. These activated P2 purinergic receptors regulate the progression of GC mainly by mediating ion channels and intracellular signal cascades. It is worth noting that there is a difference in the expression of P2 purinergic receptors in GC, which may play different roles in the progression of GC as a tumor promoting factor or a tumor suppressor factor. Among them, P2 × 7, P2Y2 and P2Y6 receptors have certain clinical significance in patients with GC and may be used as biological molecular markers for the prediction of patients with GC. Therefore, in this paper, we discuss the functional role of nucleotide / P2 purinergic receptors signal axis in regulating the progression of GC and that these P2 purinergic receptors may be used as potential molecular targets for the prevention and treatment of GC.

摘要

研究证实,P2嘌呤能受体(P2X受体和P2Y受体)在胃癌(GC)细胞和GC组织中表达,并与其功能相关。内源性核苷酸,包括ATP、ADP、UTP和UDP,作为P2嘌呤能受体激活剂,参与P2嘌呤能信号转导途径。这些激活的P2嘌呤能受体主要通过介导离子通道和细胞内信号级联反应来调节GC的进展。值得注意的是,P2嘌呤能受体在GC中的表达存在差异,其在GC进展中可能作为肿瘤促进因子或肿瘤抑制因子发挥不同作用。其中,P2×7、P2Y2和P2Y6受体在GC患者中具有一定的临床意义,可能作为预测GC患者的生物分子标志物。因此,在本文中,我们讨论了核苷酸/P2嘌呤能受体信号轴在调节GC进展中的功能作用,以及这些P2嘌呤能受体可能作为预防和治疗GC的潜在分子靶点。

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Biomed Pharmacother. 2023 Jun;162:114713. doi: 10.1016/j.biopha.2023.114713. Epub 2023 Apr 20.
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Biomed Pharmacother. 2023 Feb;158:114205. doi: 10.1016/j.biopha.2022.114205. Epub 2023 Jan 4.
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Carcinogenesis. 2023 May 15;44(1):65-79. doi: 10.1093/carcin/bgac095.
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Biomed Pharmacother. 2023 Jan;157:113927. doi: 10.1016/j.biopha.2022.113927. Epub 2022 Nov 30.
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