Effects of chloroquine on proliferation, apoptosis and autophagy of human cervical cancer cell line HeLa

Objective To investigate the effect of chloroquine (CQ) on proliferation, apoptosis and autophagy of human cervical cancer cell line HeLa and to preliminarily explore its mechanism of action. Methods HeLa cells were divided into control group and experimental groups: chloroquine-1 to chlor...

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Bibliographic Details
Main Author: GAO Peng, XU Dandan, ZHANG Bin, LIU Xuntao, SHU Lisha
Format: Article
Language:zho
Published: Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. 2023-10-01
Series:Jichu yixue yu linchuang
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Online Access:http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2023-43-10-1512.pdf
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Summary:Objective To investigate the effect of chloroquine (CQ) on proliferation, apoptosis and autophagy of human cervical cancer cell line HeLa and to preliminarily explore its mechanism of action. Methods HeLa cells were divided into control group and experimental groups: chloroquine-1 to chloroquine-5 groups (25,50,75,100, 150 μmol/L CQ respectively). The cells all were cultured for 24 and 48 h; CCK-8 and colony formation assays were used to detect cell proliferation; reactive oxygen species detection kit was used to detect intracellular ROS production; flow cytometry was used to detect apoptosis rate. The expression level of autophagy proteins p62, LC3 and Beclin1, apoptosis proteins Bax, Bcl-2 and PARP and PI3K/AKT/MDM2 pathway proteins was detected by protein immunoblotting. Results CQ inhibited cell proliferation in a time- and concentration-dependent manner (P<0.01); CQ significantly inhibited cell autophagy, induced intracellular ROS production and induced apoptosis (P<0.01). Compared with control group, CQ significantly inhibited the activation of PI3K/AKT/MDM2 signaling pathway (P<0.05). Conclusions Chloroquine may inhibit the proliferation of HeLa cells and induce apoptosis through the PI3K/AKT/MDM2 pathway.
ISSN:1001-6325