miR‐148a‐3p regulates proliferation and apoptosis of idiopathic gingival fibroma by targeting NPTX1

Author:

Sun Yuyang123ORCID,Xie Liangkun1,Ren Xiaobin1,Ran Liquan1ORCID,He Hongbing1,Kong Fanying12,Yang Shuran12,Zhang Mingzhu1ORCID

Affiliation:

1. Kunming Medical University Affiliated Stomatology Hospital Kunming China

2. Yunnan Key Laboratory of Stomatology Kunming China

3. Department of Stomatology Taihe Affiliated Hospital of Hubei University of Medicine Shiyan China

Abstract

AbstractObjectiveIdiopathic gingival fibromatosis (IGF) is a rare heterogeneous disease that results in the progressive and diffuse hyperplasia of gingival tissues. MicroRNAs are implicated in the development and progression of various tumors. The present study aimed to explore the potential roles and mechanisms of miR‐148a‐3p in IGF.MethodsGingival fibroblasts (GFs) were transfected with miR‐148a‐3p mimics, miR‐148a‐3p inhibitors, or siNPTX1, and then, the proliferation and apoptosis of GFs and the expression of related genes were evaluated using Cell Counting Kit‐8 assays, 5‐ethynyl‐2′‐deoxyuridine assays, flow cytometry, reverse transcription‐quantitative polymerase chain reaction, and western blot analysis, respectively.ResultsmiR‐148a‐3p was highly expressed in GFs of IGF (IGF‐GFs) as compared with normal GFs (N‐GFs). Overexpression of miR‐148a‐3p promoted the proliferation and inhibited the apoptosis of N‐GFs, whereas downregulation of miR‐148a‐3p had the opposite effect in IGF‐GFs. Knockdown of NPTX1 reversed miR‐148a‐3p‐mediated effects in IGF‐GFs. Dual‐luciferase reporter assay confirmed that NPTX1 is a direct target of miR‐148a‐3p.ConclusionThese findings identify that miR‐148a‐3p could regulate cell proliferation and apoptosis by targeting NPTX1, providing new insights for the further study of the molecular mechanism and treatment of IGF.

Publisher

Wiley

Subject

General Dentistry,Otorhinolaryngology

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3