GPD1L may inhibit the development of esophageal squamous cell carcinoma through the PI3K/AKT signaling pathway: bioinformatics analysis and experimental exploration.

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
LanLan Gan, Lu Zhou, ALan Chu, Chen Sun, YongTai Wang, MengLin Yang, ZongWen Liu
{"title":"GPD1L may inhibit the development of esophageal squamous cell carcinoma through the PI3K/AKT signaling pathway: bioinformatics analysis and experimental exploration.","authors":"LanLan Gan, Lu Zhou, ALan Chu, Chen Sun, YongTai Wang, MengLin Yang, ZongWen Liu","doi":"10.1007/s11033-024-10070-1","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Esophageal squamous carcinoma (ESCC) is the most prevalent pathological subtype of esophageal cancer (EC). It has the characteristics of significant local invasion, quick disease progression, high recurrence rates, and a dismal prognosis for survival. Phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) is a signaling system whose aberrant activation regulates downstream factors, leading to the promotion of cancer development. This study looks at a protein called Glycerol-3-phosphate dehydrogenase 1-like (GPD1L), which strongly affects the development of several cancers. However, its association with ESCC development and its underlying mechanisms are not clear.</p><p><strong>Methods: </strong>In this paper, we analyzed six ESCC transcriptome data obtained from the GEO database. We utilized bioinformatics technology and immunohistochemistry to differentially analyze GPD1L levels of mRNA and protein expression in ESCC and normal adjacent tissues. Furthermore, we conducted survival, co-expression, enrichment, immune infiltration and drug sensitivity analysis. Moreover, we further investigated the role and mechanism of GPD1L by Western Blot (WB), Cell Counting Kit-8 (CCK8), wound healing assay, Transwell assay, and flow cytometry. Finally, the addition of IGF-1, the activator of PI3K/AKT, could rescue the inhibitory effect of GPD1L on ESCC.</p><p><strong>Results: </strong>The findings manifest that the expression of GPD1L was low in ESCC, and functional experiments showed that GPD1L promoted apoptosis in vitro while blocking cell migration, invasion, and proliferation. Based on mechanism research, GPD1L's impact on ESCC could be explained by its suppression of the PI3K/AKT signaling pathway's activation.</p><p><strong>Conclusion: </strong>To sum up, our findings imply that GPD1L may impede the initiation and advancement of ESCC via modulating the PI3K/AKT signaling pathway. GPD1L is considered to be a promising therapeutic target and biomarker to diagnose and treat ESCC.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"51 1","pages":"1149"},"PeriodicalIF":2.6000,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Biology Reports","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s11033-024-10070-1","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Esophageal squamous carcinoma (ESCC) is the most prevalent pathological subtype of esophageal cancer (EC). It has the characteristics of significant local invasion, quick disease progression, high recurrence rates, and a dismal prognosis for survival. Phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) is a signaling system whose aberrant activation regulates downstream factors, leading to the promotion of cancer development. This study looks at a protein called Glycerol-3-phosphate dehydrogenase 1-like (GPD1L), which strongly affects the development of several cancers. However, its association with ESCC development and its underlying mechanisms are not clear.

Methods: In this paper, we analyzed six ESCC transcriptome data obtained from the GEO database. We utilized bioinformatics technology and immunohistochemistry to differentially analyze GPD1L levels of mRNA and protein expression in ESCC and normal adjacent tissues. Furthermore, we conducted survival, co-expression, enrichment, immune infiltration and drug sensitivity analysis. Moreover, we further investigated the role and mechanism of GPD1L by Western Blot (WB), Cell Counting Kit-8 (CCK8), wound healing assay, Transwell assay, and flow cytometry. Finally, the addition of IGF-1, the activator of PI3K/AKT, could rescue the inhibitory effect of GPD1L on ESCC.

Results: The findings manifest that the expression of GPD1L was low in ESCC, and functional experiments showed that GPD1L promoted apoptosis in vitro while blocking cell migration, invasion, and proliferation. Based on mechanism research, GPD1L's impact on ESCC could be explained by its suppression of the PI3K/AKT signaling pathway's activation.

Conclusion: To sum up, our findings imply that GPD1L may impede the initiation and advancement of ESCC via modulating the PI3K/AKT signaling pathway. GPD1L is considered to be a promising therapeutic target and biomarker to diagnose and treat ESCC.

GPD1L 可通过 PI3K/AKT 信号通路抑制食管鳞状细胞癌的发展:生物信息学分析和实验探索。
背景:食管鳞癌(ESCC)是食管癌(EC)中最常见的病理亚型。它具有局部浸润明显、疾病进展快、复发率高、生存预后差等特点。磷脂酰肌醇 3- 激酶/丝氨酸-苏氨酸激酶(PI3K/AKT)是一种信号系统,其异常激活会调节下游因子,从而促进癌症的发展。这项研究关注的是一种名为甘油-3-磷酸脱氢酶1-样(GPD1L)的蛋白质,它对多种癌症的发展有很大影响。然而,它与 ESCC 发展的关系及其内在机制尚不清楚:本文分析了从 GEO 数据库中获得的六种 ESCC 转录组数据。我们利用生物信息学技术和免疫组化技术对 GPD1L 在 ESCC 和正常邻近组织中的 mRNA 和蛋白表达水平进行了差异分析。此外,我们还进行了生存、共表达、富集、免疫浸润和药物敏感性分析。此外,我们还通过 Western Blot (WB)、Cell Counting Kit-8 (CCK8)、伤口愈合试验、Transwell 试验和流式细胞术进一步研究了 GPD1L 的作用和机制。最后,加入 PI3K/AKT 的激活剂 IGF-1 可以挽救 GPD1L 对 ESCC 的抑制作用:结果:研究结果表明,GPD1L在ESCC中的表达量较低,功能实验表明,GPD1L在体外促进细胞凋亡,同时阻断细胞迁移、侵袭和增殖。根据机理研究,GPD1L对ESCC的影响可以通过抑制PI3K/AKT信号通路的激活来解释:综上所述,我们的研究结果表明,GPD1L 可通过调节 PI3K/AKT 信号通路阻碍 ESCC 的发生和发展。GPD1L被认为是诊断和治疗ESCC的一个有前景的治疗靶点和生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Molecular Biology Reports
Molecular Biology Reports 生物-生化与分子生物学
CiteScore
5.00
自引率
0.00%
发文量
1048
审稿时长
5.6 months
期刊介绍: Molecular Biology Reports publishes original research papers and review articles that demonstrate novel molecular and cellular findings in both eukaryotes (animals, plants, algae, funghi) and prokaryotes (bacteria and archaea).The journal publishes results of both fundamental and translational research as well as new techniques that advance experimental progress in the field and presents original research papers, short communications and (mini-) reviews.
×
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