Acetylshikonin induces apoptosis through the endoplasmic reticulum stress‐activated PERK/eIF/CHOP axis in oesophageal squamous cell carcinoma

Author:

Yuan Ya‐Jiao12,Liu Shanshan1,Yang Hong3,Xu Jian‐Ling1ORCID,Zhai Jing1,Jiang Han‐Ming1,Sun Beibei1ORCID

Affiliation:

1. Department of Biochemistry and Molecular Biology, College of Clinical and Basic Medicine Shandong First Medical University & Shandong academy of medical sciences Jinan China

2. Department of Clinical Laboratory Qingdao Jimo People's Hospital Qingdao China

3. Department of Clinical Laboratory Taian Central Hospital China

Abstract

AbstractAcetylshikonin (AS) is an active component of Lithospermum erythrorhizon Sieb. et Zucc that exhibits activity against various cancers; however, the underlying mechanisms of AS against oesophageal squamous carcinoma (ESCC) need to be elusive. The research explores the anti‐cancer role and potential mechanism of AS on ESCC in vitro and in vivo, providing evidences for AS treatment against ESCC. In this study, we firstly demonstrated that AS treatment effectively inhibits cell viability and proliferation of ESCC cells. In addition, AS significantly induces G1/S phage arrest and promotes apoptosis in ESCC cell lines. Further studies reveal that AS induces ER stress, as observed by dose‐ and time‐dependently increased expression of BIP, PDI, PERK, phosphorylation of eIF, CHOP and splicing of XBP1. CHOP knockdown or PERK inhibition markedly rescue cell apoptosis induced by AS. Moreover, AS treatment significantly inhibits ESCC xenograft growth in nude mice. Elevated expression of BIP and CHOP is also observed in xenograft tumours. Taken together, AS inhibits proliferation and induces apoptosis through ER stress‐activated PERK/eIF/CHOP pathway in ESCC, which indicates AS represents a promising candidate for ESCC treatment.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Shandong Province

Shandong First Medical University

Publisher

Wiley

Subject

Cell Biology,Molecular 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