{"title":"miR-34a-5p通过下调CDC25A抑制宫颈癌的生长和迁移。","authors":"Tao Jiang, Hongyan Cheng","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>To define mechanisms underlying the regulation of CDC25A by miR-34a-5p in cervical cancer (CC).</p><p><strong>Methods: </strong>Quantifications of miR-34a-5p and CDC25A levels were performed in 68 CC tissues and matched controls. CC cell lines HeLa and SiHa were transfected to monitor their biological behavior changes.</p><p><strong>Results: </strong>Low-expressed miR-34a-5p and up-regulated CDC25A were noted in CC. Either overexpression of miR-34a-5p or inhibition of CDC25A blocked the growth and migration of HeLa and SiHa cells, resulting in an increase in apoptosis (p<0.05), while inhibition of miR-34a-5p or overexpression of CDC25A promoted tumor growth. Dual-luciferase reporter (DLR) assay and cell transfection identified the targeting relationship between miR-34a-5p and CDC25A, and correlation analysis revealed a negative association between them in CC. Co-transfection assays showed that overexpression of CDC25A reversed the inhibition of miR-34a-5p on CC growth and migration.</p><p><strong>Conclusion: </strong>miR-34a-5p mediates growth, migration and other malignant behaviors in CC by regulating CDC25A.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"miR-34a-5p blocks cervical cancer growth and migration by downregulating CDC25A.\",\"authors\":\"Tao Jiang, Hongyan Cheng\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>To define mechanisms underlying the regulation of CDC25A by miR-34a-5p in cervical cancer (CC).</p><p><strong>Methods: </strong>Quantifications of miR-34a-5p and CDC25A levels were performed in 68 CC tissues and matched controls. CC cell lines HeLa and SiHa were transfected to monitor their biological behavior changes.</p><p><strong>Results: </strong>Low-expressed miR-34a-5p and up-regulated CDC25A were noted in CC. Either overexpression of miR-34a-5p or inhibition of CDC25A blocked the growth and migration of HeLa and SiHa cells, resulting in an increase in apoptosis (p<0.05), while inhibition of miR-34a-5p or overexpression of CDC25A promoted tumor growth. Dual-luciferase reporter (DLR) assay and cell transfection identified the targeting relationship between miR-34a-5p and CDC25A, and correlation analysis revealed a negative association between them in CC. Co-transfection assays showed that overexpression of CDC25A reversed the inhibition of miR-34a-5p on CC growth and migration.</p><p><strong>Conclusion: </strong>miR-34a-5p mediates growth, migration and other malignant behaviors in CC by regulating CDC25A.</p>\",\"PeriodicalId\":50248,\"journal\":{\"name\":\"Journal of Buon\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Buon\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Buon","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
miR-34a-5p blocks cervical cancer growth and migration by downregulating CDC25A.
Purpose: To define mechanisms underlying the regulation of CDC25A by miR-34a-5p in cervical cancer (CC).
Methods: Quantifications of miR-34a-5p and CDC25A levels were performed in 68 CC tissues and matched controls. CC cell lines HeLa and SiHa were transfected to monitor their biological behavior changes.
Results: Low-expressed miR-34a-5p and up-regulated CDC25A were noted in CC. Either overexpression of miR-34a-5p or inhibition of CDC25A blocked the growth and migration of HeLa and SiHa cells, resulting in an increase in apoptosis (p<0.05), while inhibition of miR-34a-5p or overexpression of CDC25A promoted tumor growth. Dual-luciferase reporter (DLR) assay and cell transfection identified the targeting relationship between miR-34a-5p and CDC25A, and correlation analysis revealed a negative association between them in CC. Co-transfection assays showed that overexpression of CDC25A reversed the inhibition of miR-34a-5p on CC growth and migration.
Conclusion: miR-34a-5p mediates growth, migration and other malignant behaviors in CC by regulating CDC25A.
期刊介绍：
JBUON aims at the rapid diffusion of scientific knowledge in Oncology.
Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board.
With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world.
With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers.
JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.
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