GPD1 通过抑制线粒体功能缓解口腔癌细胞的增殖、迁移和侵袭能力

IF 1.1 4区 医学 Q4 TOXICOLOGY
Qichao Kang, Xiangling Liao, Zhen Du
{"title":"GPD1 通过抑制线粒体功能缓解口腔癌细胞的增殖、迁移和侵袭能力","authors":"Qichao Kang, Xiangling Liao, Zhen Du","doi":"10.1007/s13273-024-00445-7","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Oral cancer is a very familiar tumor together with a gravely effect on the life of human. GPD1 has been verified to join into the regulation of multifold cancers’ progression through being a suppressor. Interestingly, it has been revealed that GPD1 overexpression activated the PI3K/AKT signaling pathway. However, the regulatory functions of GPD1 on the PI3K/AKT/GSK-3β pathway in oral cancer progression keep vague, and need more investigations.</p><h3 data-test=\"abstract-sub-heading\">Objectives</h3><p>To investigate the regulation function and mechanism of GPD1 in oral cancer.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>It was demonstrated that GPD1 exhibited lower expression in oral cancer. Moreover, overexpression of GPD1 relieved cell proliferation and strengthened cell apoptosis in oral cancer. Overexpression of GPD1 weakened cell migration and invasion in oral cancer. In addition, it was confirmed that overexpression of GPD1 suppressed mitochondrial function in oral cancer. At last, it was illustrated that GPD1 triggered the PI3K/AKT/GSK-3β pathway.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>For the first time, this work manifested that GPD1 inhibited the proliferation, migration and invasion of oral cancer cells by inhibiting mitochondrial function through triggering the PI3K/AKT/GSK-3β pathway. This discovery hinted that GPD1 may be a serviceable biomarker for the treatment of oral cancer.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"67 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2024-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"GPD1 relieves the proliferation, migration and invasion abilities of oral cancer cells by inhibiting mitochondrial function\",\"authors\":\"Qichao Kang, Xiangling Liao, Zhen Du\",\"doi\":\"10.1007/s13273-024-00445-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<h3 data-test=\\\"abstract-sub-heading\\\">Background</h3><p>Oral cancer is a very familiar tumor together with a gravely effect on the life of human. GPD1 has been verified to join into the regulation of multifold cancers’ progression through being a suppressor. Interestingly, it has been revealed that GPD1 overexpression activated the PI3K/AKT signaling pathway. However, the regulatory functions of GPD1 on the PI3K/AKT/GSK-3β pathway in oral cancer progression keep vague, and need more investigations.</p><h3 data-test=\\\"abstract-sub-heading\\\">Objectives</h3><p>To investigate the regulation function and mechanism of GPD1 in oral cancer.</p><h3 data-test=\\\"abstract-sub-heading\\\">Results</h3><p>It was demonstrated that GPD1 exhibited lower expression in oral cancer. Moreover, overexpression of GPD1 relieved cell proliferation and strengthened cell apoptosis in oral cancer. Overexpression of GPD1 weakened cell migration and invasion in oral cancer. In addition, it was confirmed that overexpression of GPD1 suppressed mitochondrial function in oral cancer. At last, it was illustrated that GPD1 triggered the PI3K/AKT/GSK-3β pathway.</p><h3 data-test=\\\"abstract-sub-heading\\\">Conclusion</h3><p>For the first time, this work manifested that GPD1 inhibited the proliferation, migration and invasion of oral cancer cells by inhibiting mitochondrial function through triggering the PI3K/AKT/GSK-3β pathway. This discovery hinted that GPD1 may be a serviceable biomarker for the treatment of oral cancer.</p>\",\"PeriodicalId\":18683,\"journal\":{\"name\":\"Molecular & Cellular Toxicology\",\"volume\":\"67 1\",\"pages\":\"\"},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2024-04-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & Cellular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s13273-024-00445-7\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13273-024-00445-7","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景口腔癌是人们非常熟悉的一种肿瘤,严重影响人类的生活。GPD1 作为一种抑制因子,已被证实能参与调控多种癌症的进展。有趣的是,研究发现 GPD1 过表达会激活 PI3K/AKT 信号通路。结果表明,GPD1 在口腔癌中的表达量较低。结果表明 GPD1 在口腔癌中的表达量较低,而且过表达 GPD1 可抑制口腔癌细胞增殖并增强细胞凋亡。过量表达 GPD1 会削弱口腔癌细胞的迁移和侵袭能力。此外,还证实过量表达 GPD1 会抑制口腔癌的线粒体功能。结论本研究首次表明,GPD1 通过触发 PI3K/AKT/GSK-3β 通路,抑制线粒体功能,从而抑制口腔癌细胞的增殖、迁移和侵袭。这一发现暗示 GPD1 可能是治疗口腔癌的有效生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

GPD1 relieves the proliferation, migration and invasion abilities of oral cancer cells by inhibiting mitochondrial function

GPD1 relieves the proliferation, migration and invasion abilities of oral cancer cells by inhibiting mitochondrial function

Background

Oral cancer is a very familiar tumor together with a gravely effect on the life of human. GPD1 has been verified to join into the regulation of multifold cancers’ progression through being a suppressor. Interestingly, it has been revealed that GPD1 overexpression activated the PI3K/AKT signaling pathway. However, the regulatory functions of GPD1 on the PI3K/AKT/GSK-3β pathway in oral cancer progression keep vague, and need more investigations.

Objectives

To investigate the regulation function and mechanism of GPD1 in oral cancer.

Results

It was demonstrated that GPD1 exhibited lower expression in oral cancer. Moreover, overexpression of GPD1 relieved cell proliferation and strengthened cell apoptosis in oral cancer. Overexpression of GPD1 weakened cell migration and invasion in oral cancer. In addition, it was confirmed that overexpression of GPD1 suppressed mitochondrial function in oral cancer. At last, it was illustrated that GPD1 triggered the PI3K/AKT/GSK-3β pathway.

Conclusion

For the first time, this work manifested that GPD1 inhibited the proliferation, migration and invasion of oral cancer cells by inhibiting mitochondrial function through triggering the PI3K/AKT/GSK-3β pathway. This discovery hinted that GPD1 may be a serviceable biomarker for the treatment of oral cancer.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
2.50
自引率
17.60%
发文量
114
审稿时长
6-12 weeks
期刊介绍: Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.
×
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