Study on the mechanism of miR-361-5p regulation of androgen receptor in castration-resistant transformation of prostate cancer

Author:

Zhang Peng1,Yin Xin2,Li Xinzhao3,Zang Mingyi4,Liang Qing4,Zhang Zhiguo4,Liu Lin4,Han Conghui1,He Jie4,Liu Dachuang1

Affiliation:

1. Graduate School of Bengbu Medical University

2. Anhui Medical University

3. Fuyang Cancer Hospital

4. Xuzhou Central Hospital

Abstract

Abstract

Prostate cancer has become one of the most common tumors endangering men's health. At present, the main clinical treatments for prostate tumors are surgery, radiotherapy, endocrine therapy, chemotherapy, etc. However, due to drug resistance, the treatment effect of prostate cancer is not good, and the expression of androgen receptor (AR) and its protein structure changes play a crucial role in the resistance of prostate cancer. The expression of androgen receptor (AR) and changes in its protein structure play a crucial role in prostate cancer drug resistance. Non-coding RNAs, especially miRNAs, are involved in post-transcriptional regulation of genes and play an important role in the development of tumor cells, and may be used as specific substances to assist in the treatment of cancer. Our previous study showed that miR-361-5p expression was down-regulated in prostate cancer and that overexpression of miR-361-5p inhibited the proliferation, migration and promoted apoptosis of castration-resistant prostate cancer cells, DU145 and PC3, however, the mechanism through which miR-361-5p affects the progression of prostate cancer is unknown. We found that miR-361-5p could target binding to androgen receptor (AR) and play a role in the transformation of hormone-sensitive prostate cancer cells (LNCAP) to castration-resistant prostate cancer cells (LNCAP-AI), which inhibited proliferation, migration and promoted apoptosis of prostate cancer cells. Therefore, we suggest that miR-361-5p can target AR and inhibit the rapid growth of AR in the early stage of transformation, thus inhibiting the transformation of prostate cancer cells to castration-resistant.

Publisher

Research Square Platform LLC

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