{"title":"Regulatory effects of miR-188-5p/XRCC5 on the progression of natural killer/T-cell lymphoma.","authors":"Qianqian Huang, Siruiyun Ding, Hui Zhang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Natural killer/T cell lymphoma (NKTCL) is a malignant condition. The molecular pathological mechanism of NKTCL has not been well studied. In this article we tried to study the role of microRNA-188-5p (miR-188-5p) in NKTCL.</p><p><strong>Methods: </strong>The expression level of miR-188-5p and XRCC5 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay and colony formation assay were used to assess the ability of cell proliferation. Dual luciferase reporter assay was used to examine the down-stream target of miR-188-5p. Western blotting was utilized to determine XRCC5 expression level.</p><p><strong>Results: </strong>miR-188-5p was down-regulated in NKTCL. High expression of miR-188-5p accelerated cell proliferation. XRCC5 was one of the down-stream targets. Our data indicated that miR-188-5p suppressed NKTCL progression via regulating XRCC5 expression.</p><p><strong>Conclusions: </strong>This research elucidated that miR-188-5p suppressed tumor progression in NKTCL by regulating XRCC5. Our data may provide more evidence in looking for novel therapeutic targets.</p>","PeriodicalId":50248,"journal":{"name":"Journal of Buon","volume":" ","pages":"2033-2039"},"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}
引用次数: 0
Abstract
Purpose: Natural killer/T cell lymphoma (NKTCL) is a malignant condition. The molecular pathological mechanism of NKTCL has not been well studied. In this article we tried to study the role of microRNA-188-5p (miR-188-5p) in NKTCL.
Methods: The expression level of miR-188-5p and XRCC5 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay and colony formation assay were used to assess the ability of cell proliferation. Dual luciferase reporter assay was used to examine the down-stream target of miR-188-5p. Western blotting was utilized to determine XRCC5 expression level.
Results: miR-188-5p was down-regulated in NKTCL. High expression of miR-188-5p accelerated cell proliferation. XRCC5 was one of the down-stream targets. Our data indicated that miR-188-5p suppressed NKTCL progression via regulating XRCC5 expression.
Conclusions: This research elucidated that miR-188-5p suppressed tumor progression in NKTCL by regulating XRCC5. Our data may provide more evidence in looking for novel therapeutic targets.
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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