{"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.
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.