Circ‐DTL sponges miR‐758‐3p to accelerate cervical cancer malignant progression by regulating DCUN1D1 expression

Author:

Luo Xiaoning1,Liu Jiewen1,Wang Xiangcai1,Yuan Jun1,Zhang Yu1ORCID

Affiliation:

1. Department of Oncology, The First Affiliated Hospital of Gannan Medical University Gannan Medical University Ganzhou Jiangxi China

Abstract

AbstractCircular RNAs (circRNAs) play important roles in regulating various cancer progression. However, the function and clinical significance of circ‐denticleless E3 ubiquitin proteinligase homolog (DTL) in cervical cancer (CC) have not been studied. The present work explored the function and mechanism of circ‐DTL in CC development. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to examine the expression of circ‐DTL, miR‐758‐3p, and DCUN1D1. Cell Counting Kit‐8 (CCK‐8) and 5‐ethynyl‐2′‐deoxyuridine (EdU) assays were used to detect cell proliferation. Cell cycle and cell apoptosis were investigated by flow cytometry. Wound‐healing assay and transwell assay were conducted to assess cell migration and cell invasion. Western blot assay was carried out to determine protein expression. Dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay were used to identify the relationship between miR‐758‐3p and circ‐DTL or DCUN1D1. Xenograft mouse model assay was conducted to explore the role of circ‐DTL in CC progression in vivo. Circ‐DTL and DCUN1D1 expression were upregulated in CC tissues and CC cells, but miR‐758‐3p expression was downregulated. Knockdown of circ‐DTL inhibited CC cell growth, migration, and invasion and promoted cell cycle arrest and cell apoptosis. Circ‐DTL could sponge miR‐758‐3p to modulate CC cell progression. Moreover, miR‐758‐3p inhibited CC malignant development by suppressing DCUN1D1 expression. In addition, circ‐DTL knockdown repressed CC cell tumor properties in vivo. Circ‐DTL acted as a tumor promoter in CC development by regulating the miR‐758‐3p/DCUN1D1 pathway.

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

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