Wenqing Xu , Zhihong Zhong , Long Gu , Yiming Xiao , BinShen Chen , Weilie Hu
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The effect of circCPA4 on tumor growth was evaluated by xenotransplantation in nude mice.</p></div><div><h3>Results</h3><p>circCPA4 and SHOC2 levels were abundant while miR-491-5p expression was low in PC. Loss of circCPA4 decreased the proliferation and EdU-positive rate of PC cells, enhanced apoptosis, and inhibited invasion, migration, and EMT. Upregulation of circCPA4 forced the malignant behaviors of PC cells, and this promotion could be abolished when miR-491-5p was overexpressed or SHOC2 was silenced. CircCAP4 competitively decoyed miR-491-5p mediating SHOC2 expression. circCAP4 suppression inhibited PC tumor growth.</p></div><div><h3>Conclusion</h3><p>circCAP4 acts as a novel oncogenic factor in PC, accelerating the malignant behavior of PC cells via miR-491-5p/SHOC2 interaction. This novel ceRNA axis may be a potential target for PC drug development and targeted therapy in the future.</p></div>","PeriodicalId":10472,"journal":{"name":"Clinics","volume":null,"pages":null},"PeriodicalIF":2.2000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1807593223001503/pdfft?md5=c5311340e218d03a86de4bb020ab3e42&pid=1-s2.0-S1807593223001503-main.pdf","citationCount":"0","resultStr":"{\"title\":\"circCPA4 induces malignant behaviors of prostate cancer via miR-491-5p/SHOC2 feedback loop\",\"authors\":\"Wenqing Xu , Zhihong Zhong , Long Gu , Yiming Xiao , BinShen Chen , Weilie Hu\",\"doi\":\"10.1016/j.clinsp.2023.100314\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><p>circCPA4 has been defined to be an oncogenic gene. 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引用次数: 0
摘要
目的circCPA4已被定义为一种致癌基因。方法 收集前列腺癌组织和 PC 细胞系，通过 RT-qPCR 和免疫印迹评估 circCPA4/miR-491-5p/SHOC2 的水平。集落形成试验和 EdU 试验评估细胞增殖，流式细胞术检测细胞凋亡，Transwell 试验评估侵袭和迁移。免疫印迹法评估了 Ki-67、裂解的 Caspase-3、E-cadherin 和 N-cadherin。根据荧光素酶报告实验和RIP实验，作者研究了circCPA4/miR-491-5p/SHOC2之间的靶向关系。结果circCPA4和SHOC2水平很高，而miR-491-5p在PC中的表达很低。缺失 circCPA4 会降低 PC 细胞的增殖和 EdU 阳性率，增强细胞凋亡，抑制侵袭、迁移和 EMT。circCPA4的上调会促进PC细胞的恶性行为，而当miR-491-5p被过表达或SHOC2被沉默时，这种促进作用就会消失。CircCAP4可竞争性地诱导介导SHOC2表达的miR-491-5p，抑制CircCAP4可抑制PC肿瘤的生长。这一新型 ceRNA 轴可能是未来 PC 药物开发和靶向治疗的潜在靶点。
circCPA4 induces malignant behaviors of prostate cancer via miR-491-5p/SHOC2 feedback loop
Objective
circCPA4 has been defined to be an oncogenic gene. This study examined whether circCPA4 regulates Prostate Cancer (PC) development and revealed its molecular mechanism.
Methods
PC tissues and PC cell lines were collected, in which circCPA4/miR-491-5p/SHOC2 levels were evaluated by RT-qPCR and immunoblot. Colony formation assay and EdU assay assessed cell proliferation, flow cytometry measured apoptosis, and Transwell assessed invasion and migration. Ki-67, cleaved caspase-3, E-cadherin, and N-cadherin were evaluated by immunoblot. Based on the luciferase reporter assay and RIP assay the authors investigated the targeting relationship between circCPA4/miR-491-5p/SHOC2. The effect of circCPA4 on tumor growth was evaluated by xenotransplantation in nude mice.
Results
circCPA4 and SHOC2 levels were abundant while miR-491-5p expression was low in PC. Loss of circCPA4 decreased the proliferation and EdU-positive rate of PC cells, enhanced apoptosis, and inhibited invasion, migration, and EMT. Upregulation of circCPA4 forced the malignant behaviors of PC cells, and this promotion could be abolished when miR-491-5p was overexpressed or SHOC2 was silenced. CircCAP4 competitively decoyed miR-491-5p mediating SHOC2 expression. circCAP4 suppression inhibited PC tumor growth.
Conclusion
circCAP4 acts as a novel oncogenic factor in PC, accelerating the malignant behavior of PC cells via miR-491-5p/SHOC2 interaction. This novel ceRNA axis may be a potential target for PC drug development and targeted therapy in the future.
期刊介绍：
CLINICS is an electronic journal that publishes peer-reviewed articles in continuous flow, of interest to clinicians and researchers in the medical sciences. CLINICS complies with the policies of funding agencies which request or require deposition of the published articles that they fund into publicly available databases. CLINICS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration.
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