Evidence map›Paper›PMID 39794751›Full record

ArticleBMC cancer2025

Exploring the role of ELOVLs family in lung adenocarcinoma based on bioinformatic analysis and experimental validation.

Zihan Wang, Wenjing Cui, Long Liang, Jingge Qu, Yuqiang Pei, Danyang Li, Ying Luo, Yue Zhang, Yifan Qiu, Yongchang Sun

Abstract read
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Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Zihan Wang *Department of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Wenjing Cui *Department of Immunology and Key Laboratory of Infection and Immunity of Shandong Province & Key Laboratory for Experimental Teratology of Ministry of Education, Shandong University, Jinan, 250012, Shandong, People's Republic of China.
Long LiangDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Jingge QuDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Yuqiang PeiDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Danyang LiDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Ying LuoDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Yue ZhangDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
Yifan QiuDepartment of Respiratory, Cheeloo College of Medicine, Shandong Qianfoshan Hospital, Shandong University, Jinan, China.
Yongchang SunDepartment of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital, Peking University Health Science Center, Beijing, China. suny@bjmu.edu.cn.

Funding

National Natural Science Foundation of China 82170048
6 · The paper itself

Abstract

backgroundThe role of lipid metabolic reprogramming in the development of various types of cancer has already been established. However, the exact biological function and significance of the elongation of very-long-chain fatty acids (ELOVLs) gene family, which can affect fatty acid metabolism, is still not well understood in lung adenocarcinoma (LUAD). The aim of our study is to explore whether there are genes related to the pathogenesis of LUAD in the ELOVLs family, and even to guide clinical medication and potential prognostic indicators.

methodsGene expression profiling interactive analysis (GEPIA), human protein atlas (HPA), cBioPortal, Kaplan-Meier (KM) plotter, single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm and SubMap algorithms were utilized to analyze the role of ELOVLs in the LUAD. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis, cell counting kit-8 (CCK8), colony formation, wound healing, transwell migration assays and fatty acid metabolism detection were employed to confirm the significant role of ELOVL6 in vitro experiment.

resultsOur results revealed that mRNA expression levels of ELOVL2, ELOVL4 and ELOVL6 and protein expression levels of ELOVL5 and ELOVL6 were elevated in LUAD tissues compared to normal subjects. The low-expressing ELOVL6 group showed superior overall survival (OS) and disease-specific survival (DSS) versus the high-expressing group. Meanwhile, patients with low-ELOVL6 expression were more sensitive to the 4 representative chemotherapeutic agents. In vitro, we revealed that interfering with ELOVL6 could influence the viability, proliferation, migration capacity and fatty acid metabolism of LUAD cells (A549 and H1299).

conclusionsOur study indicated that ELOVL6 could be used as an indicator to evaluate the prognosis and therapeutic effect, and even potential therapeutic target for patients with LUAD.

Indexed as

Adenocarcinoma of LungFatty Acid ElongasesLung NeoplasmsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationComputational BiologyGene Expression ProfilingGene Expression Regulation, NeoplasticHumansPrognosisBiomarkers, TumorELOVL6 protein, humanFatty Acid ElongasesELOVLsFatty acid metabolismLung adenocarcinomaPersonalized treatmentPrognosis

Identifiers

PMID39794751
PMCPMC11720344

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.