{"title":"LINC01210/miR-124-3p轴介导的ZNF655促进胃癌的进展。","authors":"Wei Bo, Xu-Guang Wang, Min Zhang, Zhong Zhang","doi":"10.1002/kjm2.12634","DOIUrl":null,"url":null,"abstract":"<p><p>Gastric cancer (GC) is a common malignant tumor that usually originates from the epithelium of the gastric mucosa. ZNF655 was a suppressor gene of many cancers. However, the mechanism of ZNF655 in GC remains unknown. Quantitative polymerase chain reaction was used to assess the expression of ZNF655, LINC01210, and miR-124-3p. Western blotting was used to monitor ZNF655 protein expression. MTT, clone formation, transwell, and flow cytometry were all used to investigate the functions of GC cells. The interactions between ZNF655, LINC01210, and miR-124-3p were confirmed using the dual-luciferase reporter gene assay and the RIP assay. ZNF655 was highly expressed in GC cells. ZNF655 knockdown reduced GC cell viability, proliferation, migration, invasion, and induced apoptosis. The level of miR-124-3p was significantly reduced in GC cells. Besides, miR-124-3p targeted ZNF655 and inhibited its expression. MiR-124-3p mimics inhibited GC cell progression, but ZNF655 overexpression reversed these effects. Moreover, LINC01210 was found to be highly expressed in GC cells and to be able to sponge miR-124-3p. Furthermore, inhibiting miR-124-3p or increasing ZNF655 could counteract the effects of LINC01210 knockdown on GC cell development. Finally, ZNF655 promoted GC cell progression and was regulated by the LINC01210/miR-124-3p axis.</p>","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":"39 3","pages":"200-208"},"PeriodicalIF":2.7000,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"ZNF655 mediated by LINC01210/miR-124-3p axis promotes the progression of gastric cancer.\",\"authors\":\"Wei Bo, Xu-Guang Wang, Min Zhang, Zhong Zhang\",\"doi\":\"10.1002/kjm2.12634\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Gastric cancer (GC) is a common malignant tumor that usually originates from the epithelium of the gastric mucosa. ZNF655 was a suppressor gene of many cancers. However, the mechanism of ZNF655 in GC remains unknown. Quantitative polymerase chain reaction was used to assess the expression of ZNF655, LINC01210, and miR-124-3p. Western blotting was used to monitor ZNF655 protein expression. MTT, clone formation, transwell, and flow cytometry were all used to investigate the functions of GC cells. The interactions between ZNF655, LINC01210, and miR-124-3p were confirmed using the dual-luciferase reporter gene assay and the RIP assay. ZNF655 was highly expressed in GC cells. ZNF655 knockdown reduced GC cell viability, proliferation, migration, invasion, and induced apoptosis. The level of miR-124-3p was significantly reduced in GC cells. Besides, miR-124-3p targeted ZNF655 and inhibited its expression. MiR-124-3p mimics inhibited GC cell progression, but ZNF655 overexpression reversed these effects. Moreover, LINC01210 was found to be highly expressed in GC cells and to be able to sponge miR-124-3p. Furthermore, inhibiting miR-124-3p or increasing ZNF655 could counteract the effects of LINC01210 knockdown on GC cell development. Finally, ZNF655 promoted GC cell progression and was regulated by the LINC01210/miR-124-3p axis.</p>\",\"PeriodicalId\":49946,\"journal\":{\"name\":\"Kaohsiung Journal of Medical Sciences\",\"volume\":\"39 3\",\"pages\":\"200-208\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2023-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Kaohsiung Journal of Medical Sciences\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1002/kjm2.12634\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kaohsiung Journal of Medical Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/kjm2.12634","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
ZNF655 mediated by LINC01210/miR-124-3p axis promotes the progression of gastric cancer.
Gastric cancer (GC) is a common malignant tumor that usually originates from the epithelium of the gastric mucosa. ZNF655 was a suppressor gene of many cancers. However, the mechanism of ZNF655 in GC remains unknown. Quantitative polymerase chain reaction was used to assess the expression of ZNF655, LINC01210, and miR-124-3p. Western blotting was used to monitor ZNF655 protein expression. MTT, clone formation, transwell, and flow cytometry were all used to investigate the functions of GC cells. The interactions between ZNF655, LINC01210, and miR-124-3p were confirmed using the dual-luciferase reporter gene assay and the RIP assay. ZNF655 was highly expressed in GC cells. ZNF655 knockdown reduced GC cell viability, proliferation, migration, invasion, and induced apoptosis. The level of miR-124-3p was significantly reduced in GC cells. Besides, miR-124-3p targeted ZNF655 and inhibited its expression. MiR-124-3p mimics inhibited GC cell progression, but ZNF655 overexpression reversed these effects. Moreover, LINC01210 was found to be highly expressed in GC cells and to be able to sponge miR-124-3p. Furthermore, inhibiting miR-124-3p or increasing ZNF655 could counteract the effects of LINC01210 knockdown on GC cell development. Finally, ZNF655 promoted GC cell progression and was regulated by the LINC01210/miR-124-3p axis.
期刊介绍:
Kaohsiung Journal of Medical Sciences (KJMS), is the official peer-reviewed open access publication of Kaohsiung Medical University, Taiwan. The journal was launched in 1985 to promote clinical and scientific research in the medical sciences in Taiwan, and to disseminate this research to the international community. It is published monthly by Wiley. KJMS aims to publish original research and review papers in all fields of medicine and related disciplines that are of topical interest to the medical profession. Authors are welcome to submit Perspectives, reviews, original articles, short communications, Correspondence and letters to the editor for consideration.