miR-29a-5p modulates ferroptosis by targeting ferritin heavy chain FTH1 in prostate cancer

作者全名："Yang, Guang; Pan, Qi; Lu, Yang; Zhu, Junlong; Gou, Xin"

作者地址："[Yang, Guang; Zhu, Junlong; Gou, Xin] Chongqing Med Univ, Affiliated Hosp 1, Dept Urol Surg, Chongqing, Peoples R China; [Yang, Guang; Zhu, Junlong] Chongqing Med Univ, Affiliated Hosp 1, Cent Lab, Chongqing, Peoples R China; [Pan, Qi; Lu, Yang] Chongqing Hosp Tradit Chinese Med, Dept Dermatol, Chongqing, Peoples R China; [Gou, Xin] 1 Youyi Rd, Chongqing 400016, Peoples R China"

通信作者："Gou, X (通讯作者)，1 Youyi Rd, Chongqing 400016, Peoples R China."

来源：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:000947143000001

JCR分区：Q3

影响因子：2.5

年份：2023

卷号：652

期号：　

开始页：6

结束页：13

文献类型：Article

关键词：Ferroptosis; Prostate cancer; miRNAs

摘要："Ferroptosis is a kind of regulatory necrosis caused by phospholipid iron-dependent peroxidation. MiRNAs are known to play key roles in diverse biological functions. However, the molecular basis of miRNA-mediated ferroptosis in prostate cancer has not been fully stated. Here, with TCGA prostate cancer miRNA-seq data, we utilized Multivariate Cox regression analysis to prioritize potential miRNA and validated it in vitro and in vivo. We identified miR-29a-5p by TCGA prostate cancer miRNA-seq dataset. And we confirmed the expression of miR-29a-5p in prostate cancer cell lines. MiR-29a-5p knockdown reduced proliferation in PC-3 and LNCaP cells while increased Fe2 thorn and malondialdehyde (MDA) levels, the opposite phenomenon was observed with miR-29a-5p overexpression. Luciferase reporter assay showed an interaction between miR-29a-5p and Nrf2 downstream gene FTH1, subsequent rescue ex-periments also indirectly proved their direct effect. Finally, suppression of miR-29a-5p effectively inhibited tumor growth in vivo.These findings proved that the important role of miR-29a-5p in prostate cancer ferroptosis.(c) 2023 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/)."

基金机构：　

基金资助正文：