Lin Zhang, Jian Xu, Dequan Jiang, Jing Zhang, Hongyuan Li, Zhengzhong Zhao, Zhechuan Mei
{"title":"Hsa_circ_0057104 通过竞争性吸附 miR-627-5p，介导 CCND2 的表达，促进结直肠癌的恶性增殖和沃伯格效应。","authors":"Lin Zhang, Jian Xu, Dequan Jiang, Jing Zhang, Hongyuan Li, Zhengzhong Zhao, Zhechuan Mei","doi":"10.1080/02648725.2023.2199243","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>hsa_circ_0057104 (circPDK1) has been elucidated to regulate malignant behavior in pancreatic and renal cell carcinoma. The study functionally aimed at how circPDK1 modifies colorectal cancer (CRC) progression, along with its potential molecular mechanism.</p><p><strong>Methods: </strong>circPDK1 expression patterns in CRC tissues and cell lines were analyzed by RT-qPCR. circPDK1/miR-627-5p/CCND2 expression levels were changed by transient transfection. CCK-8 assay, flow cytometry, Transwell, immunoblotting, and commercial kits were utilized to measure CRC cell proliferation, apoptosis, invasion/migration, and glycolysis processes. Dual luciferase reporting assay and RIP assay were employed to evaluate the targeting relationship between circPDK1/miR-627-5p/CCND2.</p><p><strong>Results: </strong>circPDK1 was highly expressed in CRC. circPDK1 knockdown inhibited CRC cell proliferation, invasion/migration, and warburg effect and forced apoptosis. Overexpressing circPDK1 had the opposite effect. The effects of circPDK1 knockdown or circPDK1 overexpression on CRC cells were mitigated by downregulating miR-627-5p or CCND2, respectively. CircPDK1, by competitive adsorption of miR-627-5p, mediated CCND2 expression.</p><p><strong>Conclusion: </strong>CircPDK1 induces the malignant behavior of CRC by competitive adsorption of miR-627-5p mediating CCND2 expression, offering new insights into the future development of CRC-targeted drugs.</p>","PeriodicalId":55355,"journal":{"name":"Biotechnology & Genetic Engineering Reviews","volume":" ","pages":"3839-3855"},"PeriodicalIF":6.5000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hsa_circ_0057104, by competitive adsorption of miR-627-5p, mediates CCND2 expression to promote malignant proliferation and Warburg effect of colorectal cancer.\",\"authors\":\"Lin Zhang, Jian Xu, Dequan Jiang, Jing Zhang, Hongyuan Li, Zhengzhong Zhao, Zhechuan Mei\",\"doi\":\"10.1080/02648725.2023.2199243\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>hsa_circ_0057104 (circPDK1) has been elucidated to regulate malignant behavior in pancreatic and renal cell carcinoma. The study functionally aimed at how circPDK1 modifies colorectal cancer (CRC) progression, along with its potential molecular mechanism.</p><p><strong>Methods: </strong>circPDK1 expression patterns in CRC tissues and cell lines were analyzed by RT-qPCR. circPDK1/miR-627-5p/CCND2 expression levels were changed by transient transfection. CCK-8 assay, flow cytometry, Transwell, immunoblotting, and commercial kits were utilized to measure CRC cell proliferation, apoptosis, invasion/migration, and glycolysis processes. Dual luciferase reporting assay and RIP assay were employed to evaluate the targeting relationship between circPDK1/miR-627-5p/CCND2.</p><p><strong>Results: </strong>circPDK1 was highly expressed in CRC. circPDK1 knockdown inhibited CRC cell proliferation, invasion/migration, and warburg effect and forced apoptosis. Overexpressing circPDK1 had the opposite effect. The effects of circPDK1 knockdown or circPDK1 overexpression on CRC cells were mitigated by downregulating miR-627-5p or CCND2, respectively. CircPDK1, by competitive adsorption of miR-627-5p, mediated CCND2 expression.</p><p><strong>Conclusion: </strong>CircPDK1 induces the malignant behavior of CRC by competitive adsorption of miR-627-5p mediating CCND2 expression, offering new insights into the future development of CRC-targeted drugs.</p>\",\"PeriodicalId\":55355,\"journal\":{\"name\":\"Biotechnology & Genetic Engineering Reviews\",\"volume\":\" \",\"pages\":\"3839-3855\"},\"PeriodicalIF\":6.5000,\"publicationDate\":\"2024-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biotechnology & Genetic Engineering Reviews\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1080/02648725.2023.2199243\",\"RegionNum\":3,\"RegionCategory\":\"工程技术\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/5/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biotechnology & Genetic Engineering Reviews","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1080/02648725.2023.2199243","RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/5/2 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
Hsa_circ_0057104, by competitive adsorption of miR-627-5p, mediates CCND2 expression to promote malignant proliferation and Warburg effect of colorectal cancer.
Objective: hsa_circ_0057104 (circPDK1) has been elucidated to regulate malignant behavior in pancreatic and renal cell carcinoma. The study functionally aimed at how circPDK1 modifies colorectal cancer (CRC) progression, along with its potential molecular mechanism.
Methods: circPDK1 expression patterns in CRC tissues and cell lines were analyzed by RT-qPCR. circPDK1/miR-627-5p/CCND2 expression levels were changed by transient transfection. CCK-8 assay, flow cytometry, Transwell, immunoblotting, and commercial kits were utilized to measure CRC cell proliferation, apoptosis, invasion/migration, and glycolysis processes. Dual luciferase reporting assay and RIP assay were employed to evaluate the targeting relationship between circPDK1/miR-627-5p/CCND2.
Results: circPDK1 was highly expressed in CRC. circPDK1 knockdown inhibited CRC cell proliferation, invasion/migration, and warburg effect and forced apoptosis. Overexpressing circPDK1 had the opposite effect. The effects of circPDK1 knockdown or circPDK1 overexpression on CRC cells were mitigated by downregulating miR-627-5p or CCND2, respectively. CircPDK1, by competitive adsorption of miR-627-5p, mediated CCND2 expression.
Conclusion: CircPDK1 induces the malignant behavior of CRC by competitive adsorption of miR-627-5p mediating CCND2 expression, offering new insights into the future development of CRC-targeted drugs.
期刊介绍：
Biotechnology & Genetic Engineering Reviews publishes major invited review articles covering important developments in industrial, agricultural and medical applications of biotechnology.
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