Apigenin 7-glucoside impedes hypoxia-induced malignant phenotypes of cervical cancer cells in a p16-dependent manner

Author:

Li Yan1,Man Xiaoli2,Zhang Qing3,Wang Xiaowu4,Yang Yongli5

Affiliation:

1. Department of Gynecologic Oncology, The Affiliated Hospital of Qinghai University & Affiliated Cancer Hospital of Qinghai University , Xining , China

2. Department of Gynecology, Puyang Maternity and Child Care Centers , Puyang , China

3. Department of Gynecology and Obstetrics, The People’s Hospital of Luyi , Luyi , China

4. Department of Surgical Oncology, The Affiliated Hospital of Qinghai University , No. 29, Tongren Road , Xining , 810000 , China

5. Department of Gynecology, The Affiliated Hospital of Qinghai University & Affiliated Cancer Hospital of Qinghai University , No. 29, Tongren Road , Xining , 810000 , China

Abstract

Abstract Apigenin 7-glucoside (A7G) can suppress cell proliferation and trigger apoptosis in cervical cancer cells. Considering that hypoxia is associated with the malignant phenotypes in cervical cancer, this study aimed to uncover whether A7G exhibits suppressive effects on the hypoxia-induced malignant phenotype of cervical cancer cells (HeLa cells). Compared to normoxia, hypoxia can enhance the malignant phenotypes of HeLa cells, including cell proliferation, reduced sensitivity against chemotherapeutic agents (oxaliplatin and paclitaxel), cancer stemness, migration, and invasion. A7G intervention (20, 40, and 60 μM) could impair these malignant phenotypes of HeLa cells and upregulate the expression level of total and nuclear p16 proteins. Molecular docking analysis showed the interaction between anion exchanger 1 and A7G. In p16-silencing HeLa cells, the anticancer effects of A7G were absent. Therefore, hypoxia derives malignant phenotypes of HeLa cells, which could be impeded by A7G in a p16-dependent manner.

Publisher

Walter de Gruyter GmbH

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