P3H4 Regulates Apoptosis and Autophagy of Breast Cancer Cells via BCL-2/BAX/Caspase-3 and AMPK/mTOR/ULK1 Signaling Pathways

IF 1.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Molecular Biology Pub Date : 2024-05-02 DOI:10.1134/s0026893324700237
T. Wang, M. M. Li, Z. Dong, D. M. Zhu
{"title":"P3H4 Regulates Apoptosis and Autophagy of Breast Cancer Cells via BCL-2/BAX/Caspase-3 and AMPK/mTOR/ULK1 Signaling Pathways","authors":"T. Wang, M. M. Li, Z. Dong, D. M. Zhu","doi":"10.1134/s0026893324700237","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>The role of prolyl 3-hydroxylase family member 4 (P3H4, or SC65) in breast cancer and the molecular mechanisms in which this protein was involved were investigated. For this purpose, microchips with cancerous and paracancerous tissues collected from 56 patients with breast cancer were constructed. The P3H4 protein expression was evaluated by immunohistochemistry. Cell lines with decreased and increased P3H4 expression were selected and divided into five groups: <i>P3H4</i> overexpression and corresponding negative control, <i>P3H4</i> knockout groups #1 and #2 and corresponding negative control. CCK8 assay, colony formation test, immunoblotting, scratch test, transwell test and flow cytometry were used to determine the relevant cell functions. P3H4 expression was higher in breast cancer cells than in paracancerous tissue. Compared with corresponding negative control, proliferative activity of the cells was inhibited at 24, 48 and 72 h, migration activity and invasion ability of the cells were reduced, autophagy and apoptosis in the cells were increased in <i>P3H4</i> knockout groups #1 and #2. <i>P3H4</i> knockout promoted apoptosis of breast cancer cells and inhibited their proliferation, migration, and invasion by activating the BCL-2/BAX/Caspase-3 and AMPK/mTOR pathways. <i>P3H4</i> knockout promoted apparently autophagy by activating the AMPK/mTOR/ULK1 pathway. However, <i>P3H4</i> overexpression could promote the proliferation, migration and invasion of breast cancer cells, and inhibited apoptosis and autophagy of mammary gland adenocarcinoma cells MDA-MB-231.</p>","PeriodicalId":18734,"journal":{"name":"Molecular Biology","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1134/s0026893324700237","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The role of prolyl 3-hydroxylase family member 4 (P3H4, or SC65) in breast cancer and the molecular mechanisms in which this protein was involved were investigated. For this purpose, microchips with cancerous and paracancerous tissues collected from 56 patients with breast cancer were constructed. The P3H4 protein expression was evaluated by immunohistochemistry. Cell lines with decreased and increased P3H4 expression were selected and divided into five groups: P3H4 overexpression and corresponding negative control, P3H4 knockout groups #1 and #2 and corresponding negative control. CCK8 assay, colony formation test, immunoblotting, scratch test, transwell test and flow cytometry were used to determine the relevant cell functions. P3H4 expression was higher in breast cancer cells than in paracancerous tissue. Compared with corresponding negative control, proliferative activity of the cells was inhibited at 24, 48 and 72 h, migration activity and invasion ability of the cells were reduced, autophagy and apoptosis in the cells were increased in P3H4 knockout groups #1 and #2. P3H4 knockout promoted apoptosis of breast cancer cells and inhibited their proliferation, migration, and invasion by activating the BCL-2/BAX/Caspase-3 and AMPK/mTOR pathways. P3H4 knockout promoted apparently autophagy by activating the AMPK/mTOR/ULK1 pathway. However, P3H4 overexpression could promote the proliferation, migration and invasion of breast cancer cells, and inhibited apoptosis and autophagy of mammary gland adenocarcinoma cells MDA-MB-231.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
P3H4 通过 BCL-2/BAX/Caspase-3 和 AMPK/mTOR/ULK1 信号通路调控乳腺癌细胞的凋亡和自噬作用
摘要 研究了脯氨酰 3-羟化酶家族成员 4(P3H4,或 SC65)在乳腺癌中的作用以及该蛋白参与其中的分子机制。为此,研究人员用从 56 名乳腺癌患者身上采集的癌组织和癌旁组织构建了微芯片。免疫组化法评估了 P3H4 蛋白的表达。筛选出 P3H4 表达减少和增加的细胞系,并将其分为五组:P3H4过表达组和相应的阴性对照组、P3H4基因敲除1号和2号组及相应的阴性对照组。采用 CCK8 检测、集落形成试验、免疫印迹、划痕试验、透孔试验和流式细胞术测定相关细胞功能。P3H4在乳腺癌细胞中的表达高于癌旁组织。与相应的阴性对照组相比,P3H4 基因敲除 1 号和 2 号组在 24、48 和 72 h 内细胞的增殖活性受到抑制,细胞的迁移活性和侵袭能力降低,细胞的自噬和凋亡增加。P3H4基因敲除通过激活BCL-2/BAX/Caspase-3和AMPK/mTOR通路,促进乳腺癌细胞凋亡并抑制其增殖、迁移和侵袭。通过激活 AMPK/mTOR/ULK1 通路,P3H4 基因敲除明显促进了自噬。然而,P3H4过表达可促进乳腺癌细胞的增殖、迁移和侵袭,并抑制乳腺腺癌细胞MDA-MB-231的凋亡和自噬。
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 去求助
来源期刊
Molecular Biology
Molecular Biology 生物-生化与分子生物学
CiteScore
1.30
自引率
8.30%
发文量
78
审稿时长
3 months
期刊介绍: Molecular Biology is an international peer reviewed journal that covers a wide scope of problems in molecular, cell and computational biology including genomics, proteomics, bioinformatics, molecular virology and immunology, molecular development biology, molecular evolution and related areals. Molecular Biology publishes reviews, experimental and theoretical works. Every year, the journal publishes special issues devoted to most rapidly developing branches of physical-chemical biology and to the most outstanding scientists.
期刊最新文献
Triosephosphate Isomerase Inhibition by Resveratrol: A New Mechanism of Anti-Glycolysis in Breast Cancer Silencing of the S-Phase Kinase-Associated Protein 2 Gene (SKP2) Inhibits Proliferation and Migration of Hepatocellular Carcinoma Cells New Epigenetic Markers of Age-Dependent Changes in the Cardiovascular System Amino Acid Substitution Patterns in the E6 and E7 Proteins of HPV Type 16: Phylogeography and Evolution Human eRF1 Translation Regulation
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1