Paiteling induces apoptosis of cervical cancer cells by down-regulation of the E6/E7-Pi3k/Akt pathway: A network pharmacology

小桶 PI3K/AKT/mTOR通路 蛋白激酶B 细胞凋亡 赫拉 癌症研究 生物 宫颈上皮内瘤变 免疫印迹 细胞生长 细胞 化学 癌症 分子生物学 宫颈癌 基因表达 基因 遗传学 转录组
作者
Yunhua Liu,Pengfei Zheng,Tingting Jiao,Mengmeng Zhang,Yingjie Wu,Xinjiang Zhang,Shuyue Wang,Zongjiang Zhao
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:305: 116062-116062 被引量:7
标识
DOI:10.1016/j.jep.2022.116062
摘要

Human papillomavirus (HPV) infection is considered to be the main pathogen causing intraepithelial neoplasia. Paiteling (PTL) has been used to treat intraepithelial neoplasia caused by human papillomavirus (HPV) infection for more than 20 years in China, but its specific mechanism of action is not very clear, and further research is still needed.This study designed a comprehensive strategy to study the pharmacological mechanism of paiteling in regulating cervical cancer cell apoptosis by integrating LC-MS/MS, network pharmacology and pharmacological experiments.We used liquid chromatography-tandem mass spectrometry to detect the active substances in PTL and performed protein-protein interaction analysis on the intersection of the targets of these key compounds and the targets of intraepithelial neoplasia. Additionally, by using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes (KEGG), the potential pathway of PTL against HPV-induced intraepithelial neoplasia was predicted. Finally, we used HeLa and Ect1/E6E7 cells for experimental verification.The protein-protein interaction network predicted that AKT1, TP53, MYC, STAT3, MTOR, and MAPK were pivotal targets for PTL to inhibit epithelial neoplasia. KEGG enrichment analysis showed that the Pi3k/Akt pathway and HPV infection had scientific significance. Compared to the control group, after PTL diluent stimulated HeLa and Ect1/E6E7 cells for 24 h, cell viability, migration, and invasion capabilities were significantly reduced, and cell apoptosis was significantly increased, conforming to a dose-effect relationship and time-effect relationship. PCR, cellular immunohistochemistry, and western blot experiments showed that PTL reduced the expression of E6, Pi3k, E7, Akt, Bcl-xl, while increasing the expression of Bad in HeLa and Ect1/E6E7 cells.PTL can induce cervical cancer cell apoptosis by inhibiting the E6/E7-Pi3k/Akt signaling pathway. It may provide an effective alternative strategy of traditional Chinese medicine for the treatment of epithelial neoplasia caused by HPV infection.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
斯文败类应助火龙果采纳,获得10
刚刚
1秒前
1秒前
1秒前
1秒前
2秒前
2秒前
淀粉肠发布了新的文献求助10
2秒前
Alan发布了新的文献求助10
3秒前
3秒前
张张张完成签到 ,获得积分10
4秒前
TiuTiu关注了科研通微信公众号
4秒前
纯真书兰完成签到,获得积分10
5秒前
严昌发布了新的文献求助10
5秒前
DD完成签到,获得积分10
5秒前
ChengxinXie完成签到,获得积分20
5秒前
Hannah发布了新的文献求助10
5秒前
lss发布了新的文献求助10
6秒前
万能图书馆应助策略采纳,获得10
6秒前
陆仓颉完成签到,获得积分10
7秒前
花生发布了新的文献求助10
7秒前
今后应助缓慢修杰采纳,获得10
7秒前
小二郎应助知了采纳,获得10
7秒前
富贵儿发布了新的文献求助10
8秒前
8秒前
tyler2000完成签到,获得积分10
9秒前
shan完成签到,获得积分10
9秒前
乐乐应助xiaomili采纳,获得10
10秒前
婷崽加油完成签到,获得积分10
10秒前
南风发布了新的文献求助10
10秒前
拉长的问晴完成签到,获得积分10
11秒前
loin完成签到,获得积分10
12秒前
12秒前
抹茶泡泡完成签到 ,获得积分10
12秒前
tyler2000发布了新的文献求助10
13秒前
南至发布了新的文献求助10
13秒前
13秒前
斯文败类应助L3213036054采纳,获得10
14秒前
shan发布了新的文献求助10
14秒前
橙子发布了新的文献求助30
14秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
Handbook of Marine Craft Hydrodynamics and Motion Control, 2nd Edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3986953
求助须知:如何正确求助?哪些是违规求助? 3529326
关于积分的说明 11244328
捐赠科研通 3267695
什么是DOI,文献DOI怎么找? 1803880
邀请新用户注册赠送积分活动 881223
科研通“疑难数据库(出版商)”最低求助积分说明 808620