Circ_0005397 inhibits ferroptosis of pancreatic cancer cells by up‐regulating PCBP2 through KAT6A/H3K9Ac

Author:

Qu Tengfei12ORCID,Cha Lichao12ORCID,Liu Hongliang3ORCID,Tian Lantian12ORCID,Hu Xiao1ORCID,Zou Hao1ORCID,Feng Yujie1ORCID,Sun Chuandong1ORCID,Cao Jingyu1ORCID,Guo Weidong12ORCID,Qiu Fabo12ORCID,Zhou Bin12ORCID

Affiliation:

1. Department of Hepatobiliary and Pancreatic Surgery the Affiliated Hospital of Qingdao University Qingdao China

2. Department of Retroperitoneal Tumor Surgery the Affiliated Hospital of Qingdao University Qingdao China

3. Department of Hepatobiliary Surgery Qingdao Women's and Children's Hospital Qingdao China

Abstract

AbstractPancreatic cancer is a highly aggressive and lethal carcinoma. Circular RNAs (circRNAs) serve key regulatory functions in pancreatic cancer. Ferroptosis was induced by erastin treatment and analyzed by examining malondialdehyde (MDA), iron, Fe2+ and glutathione (GSH). C11‐BODIPY 581/591 was used to stain cells for analyzing lipid peroxidation. RNA immunoprecipitation, pull‐down and chromatin immunoprecipitation assays were applied to evaluate intermolecular interaction. Mice received subcutaneous injection of pancreatic cancer cells as a model of subcutaneous tumor for in vivo tests. Circ_0005397 was abundantly expressed in pancreatic cancer, and its upregulation was associated with low survival of patients with pancreatic cancer. Circ_0005397 expression was induced by EIF4A3. PCBP2 was highly expressed in pancreatic cancer, and circ_0005397 and PCBP2 were positively correlated in patients with pancreatic cancer. Circ_0005397 knockdown sensitized pancreatic carcinoma cells to ferroptosis via downregulating PCBP2. Circ_0005397 promoted PCBP2 transcription via facilitating the binding of KAT6A and H3K9ac to PCBP2 promoter. Silencing of circ_0005397 reduced tumor growth by enhancing erastin‐induced ferroptosis in vivo. EIF4A3‐induced circ_0005397 inhibited erastin‐induced ferroptosis in pancreatic cancer by promoting PCBP2 expression through KAT6A and H3K9ac.

Publisher

Wiley

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