RASGEF1C affects aerobic glycolysis and facilitates lung cancer progression through the PLK1 signaling pathway.

IF 2.8 3区 医学 Q2 ONCOLOGY
Expert Review of Anticancer Therapy Pub Date : 2025-08-01 Epub Date: 2025-06-23 DOI:10.1080/14737140.2025.2518278
Hao Wu, Kang Zheng, Fei Han
{"title":"RASGEF1C affects aerobic glycolysis and facilitates lung cancer progression through the PLK1 signaling pathway.","authors":"Hao Wu, Kang Zheng, Fei Han","doi":"10.1080/14737140.2025.2518278","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>RasGEF domain family member 1C (RASGEF1C), primarily acting in neurological disorders, remains largely enigmatic regarding its function in lung cancer (LC).</p><p><strong>Methods: </strong>Bioinformatics analysis assessed the differential expression and prognosis of RASGEF1C in LC and analyzed the enriched pathways. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot (WB) analyses were employed to assess the expression of RASGEF1C and polo-like kinase 1 (PLK1). Biological functions were detected by cell counting kit-8 (CCK-8), flow cytometry, colony formation assay, cell scratch assay, and Transwell assay. Glycolysis-related proteins were detected by Western blot, and ATP levels, glucose content, lactate production, extracellular acidification rate, and oxygen consumption rate were measured to assess glycolysis flux changes in a mouse xenograft tumor model. Immunohistochemistry was applied to detect levels of RASGEF1C, PLK1, and Ki67. WB was employed to assess the expression of RASGEF1C, PLK1, pyruvate kinase M2 (PKM2), and hexokinase 2 (HK2).</p><p><strong>Results: </strong>The upregulation of RASGEF1C in LC reinforced the malignant progression of tumors (<i>p</i> < 0.01). RASGEF1C activation of the PLK1 pathway enhanced aerobic glycolysis, promoting proliferation, migration, and anti-apoptotic behaviors in LC cells.</p><p><strong>Conclusions: </strong>RASGEF1C affects aerobic glycolysis through the PLK1 signaling pathway, thereby acting as a pro-cancer factor driving LC progression.</p>","PeriodicalId":12099,"journal":{"name":"Expert Review of Anticancer Therapy","volume":" ","pages":"961-971"},"PeriodicalIF":2.8000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert Review of Anticancer Therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/14737140.2025.2518278","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/23 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: RasGEF domain family member 1C (RASGEF1C), primarily acting in neurological disorders, remains largely enigmatic regarding its function in lung cancer (LC).

Methods: Bioinformatics analysis assessed the differential expression and prognosis of RASGEF1C in LC and analyzed the enriched pathways. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot (WB) analyses were employed to assess the expression of RASGEF1C and polo-like kinase 1 (PLK1). Biological functions were detected by cell counting kit-8 (CCK-8), flow cytometry, colony formation assay, cell scratch assay, and Transwell assay. Glycolysis-related proteins were detected by Western blot, and ATP levels, glucose content, lactate production, extracellular acidification rate, and oxygen consumption rate were measured to assess glycolysis flux changes in a mouse xenograft tumor model. Immunohistochemistry was applied to detect levels of RASGEF1C, PLK1, and Ki67. WB was employed to assess the expression of RASGEF1C, PLK1, pyruvate kinase M2 (PKM2), and hexokinase 2 (HK2).

Results: The upregulation of RASGEF1C in LC reinforced the malignant progression of tumors (p < 0.01). RASGEF1C activation of the PLK1 pathway enhanced aerobic glycolysis, promoting proliferation, migration, and anti-apoptotic behaviors in LC cells.

Conclusions: RASGEF1C affects aerobic glycolysis through the PLK1 signaling pathway, thereby acting as a pro-cancer factor driving LC progression.

RASGEF1C通过PLK1信号通路影响有氧糖酵解并促进肺癌进展。
目的:RasGEF结构域家族成员1C (RASGEF1C)主要作用于神经系统疾病,但其在肺癌(LC)中的功能仍是一个谜。方法:采用生物信息学方法评估RASGEF1C在LC中的差异表达及预后,分析其富集途径。采用定量逆转录聚合酶链反应(qRT-PCR)和western blot (WB)分析RASGEF1C和polo样激酶1 (PLK1)的表达。采用细胞计数试剂盒-8 (CCK-8)、流式细胞术、集落形成实验、细胞划痕实验和Transwell实验检测生物学功能。Western blot检测糖酵解相关蛋白,并测定ATP水平、葡萄糖含量、乳酸产量、细胞外酸化速率和耗氧量,以评估小鼠异种移植肿瘤模型中糖酵解通量的变化。应用免疫组织化学检测RASGEF1C、PLK1和Ki67水平。WB检测RASGEF1C、PLK1、丙酮酸激酶M2 (PKM2)和己糖激酶2 (HK2)的表达。结论:RASGEF1C通过PLK1信号通路影响有氧糖酵解,从而作为促癌因子驱动LC进展。
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
5.10
自引率
3.00%
发文量
100
审稿时长
4-8 weeks
期刊介绍: Expert Review of Anticancer Therapy (ISSN 1473-7140) provides expert appraisal and commentary on the major trends in cancer care and highlights the performance of new therapeutic and diagnostic approaches. Coverage includes tumor management, novel medicines, anticancer agents and chemotherapy, biological therapy, cancer vaccines, therapeutic indications, biomarkers and diagnostics, and treatment guidelines. All articles are subject to rigorous peer-review, and the journal makes an essential contribution to decision-making in cancer care. Comprehensive coverage in each review is complemented by the unique Expert Review format and includes the following sections: Expert Opinion - a personal view of the data presented in the article, a discussion on the developments that are likely to be important in the future, and the avenues of research likely to become exciting as further studies yield more detailed results Article Highlights – an executive summary of the author’s most critical points.
×
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:604180095
Book学术官方微信