Sodium selenite inhibits the growth of cervical cancer cells through the PI3K/AKT pathway

IF 3.6 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yuanyuan Wang , Lei Qi , Sihong Guo , Yuehui Jia , Ruixiang Wang , Cunqi Lv , Qingyu Zeng , Ying Gao , Tong Wang , Qi Li
{"title":"Sodium selenite inhibits the growth of cervical cancer cells through the PI3K/AKT pathway","authors":"Yuanyuan Wang ,&nbsp;Lei Qi ,&nbsp;Sihong Guo ,&nbsp;Yuehui Jia ,&nbsp;Ruixiang Wang ,&nbsp;Cunqi Lv ,&nbsp;Qingyu Zeng ,&nbsp;Ying Gao ,&nbsp;Tong Wang ,&nbsp;Qi Li","doi":"10.1016/j.jtemb.2024.127582","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Selenium can inhibit cervical cancers, but the specific mechanism of anti-cervical cancer is not fully understood.</div></div><div><h3>Methods</h3><div>In this study, we investigated the anti-cervical cancer effect of sodium selenite (SS) in vivo and in vitro to reveal the role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway in terms of the mechanism. In vivo experiments, HeLa cell xenografts were constructed in BALB/c female nude mice, and then intraperitoneally injected with 3 mg/kg sodium selenite (SS) for 14 days. In vitro experiments, we detected cell viability by MTT assay and apoptosis by Annexin V-FITC/PI staining. The levels of PI3K, AKT, phosphorylated PI3K (p-PI3K), and phosphorylated Akt (p-AKT) were measured by Western Blot.</div></div><div><h3>Results</h3><div>HeLa cell xenografts in female nude mice showed delayed tumor growth and no apparent toxicity in the liver or kidney. SS reduced the viability and increased apoptosis of HeLa and SiHa cells. SS did not affect PI3K and AKT levels and decreased p-PI3K and p-AKT levels. In addition, the results also revealed that the SS combined with LY294002, a specific PI3K inhibitor, enhanced the inhibitory effect of SS on the PI3K/AKT signaling pathway, further inhibiting cervical cancer cell viability and increased apoptosis.</div></div><div><h3>Conclusions</h3><div>SS exerted its anti-cervical cancer effects by inhibiting cell proliferation, promoting apoptosis, and inhibiting the PI3K/AKT signaling pathway.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127582"},"PeriodicalIF":3.6000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Trace Elements in Medicine and Biology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0946672X24002025","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background

Selenium can inhibit cervical cancers, but the specific mechanism of anti-cervical cancer is not fully understood.

Methods

In this study, we investigated the anti-cervical cancer effect of sodium selenite (SS) in vivo and in vitro to reveal the role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway in terms of the mechanism. In vivo experiments, HeLa cell xenografts were constructed in BALB/c female nude mice, and then intraperitoneally injected with 3 mg/kg sodium selenite (SS) for 14 days. In vitro experiments, we detected cell viability by MTT assay and apoptosis by Annexin V-FITC/PI staining. The levels of PI3K, AKT, phosphorylated PI3K (p-PI3K), and phosphorylated Akt (p-AKT) were measured by Western Blot.

Results

HeLa cell xenografts in female nude mice showed delayed tumor growth and no apparent toxicity in the liver or kidney. SS reduced the viability and increased apoptosis of HeLa and SiHa cells. SS did not affect PI3K and AKT levels and decreased p-PI3K and p-AKT levels. In addition, the results also revealed that the SS combined with LY294002, a specific PI3K inhibitor, enhanced the inhibitory effect of SS on the PI3K/AKT signaling pathway, further inhibiting cervical cancer cell viability and increased apoptosis.

Conclusions

SS exerted its anti-cervical cancer effects by inhibiting cell proliferation, promoting apoptosis, and inhibiting the PI3K/AKT signaling pathway.
亚硒酸钠通过PI3K/AKT通路抑制宫颈癌细胞的生长。
背景:硒具有抑制宫颈癌的作用,但其抗宫颈癌的具体机制尚不完全清楚。方法:本研究通过对亚硒酸钠(SS)体内外抗宫颈癌作用的研究,揭示其作用于磷脂酰肌醇3-激酶/蛋白激酶B (PI3K/AKT)信号通路的机制。在体内实验中,在BALB/c雌性裸鼠体内构建HeLa细胞异种移植物,然后腹腔注射3 mg/kg亚硒酸钠(SS) 14 d。体外实验采用MTT法检测细胞活力,Annexin V-FITC/PI染色检测细胞凋亡。Western Blot检测PI3K、AKT、磷酸化PI3K (p-PI3K)、磷酸化AKT (p-AKT)水平。结果:雌性裸鼠HeLa细胞异种移植后肿瘤生长延迟,对肝脏和肾脏无明显毒性。SS降低HeLa和SiHa细胞活力,增加细胞凋亡。SS不影响PI3K和AKT水平,但降低了p-PI3K和p-AKT水平。此外,研究结果还显示,SS联合特异性PI3K抑制剂LY294002可增强SS对PI3K/AKT信号通路的抑制作用,进一步抑制宫颈癌细胞活力,增加凋亡。结论:SS通过抑制细胞增殖、促进细胞凋亡、抑制PI3K/AKT信号通路发挥抗宫颈癌作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
6.60
自引率
2.90%
发文量
202
审稿时长
85 days
期刊介绍: The journal provides the reader with a thorough description of theoretical and applied aspects of trace elements in medicine and biology and is devoted to the advancement of scientific knowledge about trace elements and trace element species. Trace elements play essential roles in the maintenance of physiological processes. During the last decades there has been a great deal of scientific investigation about the function and binding of trace elements. The Journal of Trace Elements in Medicine and Biology focuses on the description and dissemination of scientific results concerning the role of trace elements with respect to their mode of action in health and disease and nutritional importance. Progress in the knowledge of the biological role of trace elements depends, however, on advances in trace elements chemistry. Thus the Journal of Trace Elements in Medicine and Biology will include only those papers that base their results on proven analytical methods. Also, we only publish those articles in which the quality assurance regarding the execution of experiments and achievement of results is guaranteed.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信