Evidence map›Paper›PMID 40183277›Full record

ArticleCombinatorial chemistry & high throughput screening2026

Metformin Inhibits the Development of Lung Adenocarcinoma by Regulating the Expression of CCNA2

Luyao Wang, Yinlong Huang, Mei Tian, Mengling Hu, Kai Zhang, Chaoqun Lian, Xiaojing Wang, Jing Zhang

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Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Luyao WangAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, Department of Pulmonary and Critical Care Medicine, Molecular Diagnosis Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233030, China.
Yinlong HuangDepartment of Genetics, School of Life Sciences, Bengbu Medical University, Bengbu, 233030, China.
Mei TianAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, Department of Pulmonary and Critical Care Medicine, Molecular Diagnosis Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233030, China.
Mengling HuDepartment of Genetics, School of Life Sciences, Bengbu Medical University, Bengbu, 233030, China.
Kai ZhangDepartment of Clinical Medicine, Bengbu Medical University, Bengbu, 233030, China.
Chaoqun LianResearch Center of Clinical Laboratory Science, Bengbu Medical University, Bengbu, 233030, China.
Xiaojing WangAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, Department of Pulmonary and Critical Care Medicine, Molecular Diagnosis Center, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233030, China.
Jing ZhangDepartment of Genetics, School of Life Sciences, Bengbu Medical University, Bengbu, 233030, China.

Funding

Anhui Provincial Major Science and Technology Project for Key Laboratory S202305a12020038Anhui Provincial Undergraduate Innovative Training Program S202410367002Key Natural Science Project of Anhui Provincial Education Department KJ2020A0578National Innovation Program for College Students 202210367076Open Research Fund Project of Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease HX2023D01, HX2023D02Open Research Fund Project of Anhui Province Key Laboratory of immunology in Chronic Diseases KLICD-2023-Z4Research Funds of Joint Research Center for Regional Diseases of Institute of Health and Medicine (IHM), Hefei Comprehensive National Science Center 2023bydjk001
6 · The paper itself

Abstract

backgroundThe incidence and mortality rates of lung cancer in China have significantly increased in recent years, and lung adenocarcinoma (LUAD) accounts for about 40% of all lung cancers. Metformin (MET) has been used as a therapeutic drug for type 2 diabetes, and a recent study revealed that MET can play an anti-tumor role by inhibiting cell proliferation, but its specific mechanism of action in LUAD is still unclear.

methodsThe key genes and signaling pathways of MET acting on LUAD were screened by bioinformatics, and the effects of MET on LUAD cell proliferation, invasion, migration, and apoptosis were detected. We then constructed small interfering RNAs for CCNA2 and combined them with MET to verify whether MET inhibits LUAD cell growth by affecting the expression of CCNA2. The binding ability of MET to E2F1 was predicted by molecular docking, and the correlation between E2F1 and CCNA2 was analyzed by bioinformatics. Finally, it was verified by interfering with the expression of E2F1 whether MET down-regulated the expression of CCNA2 by regulating E2F1, thus exerting anti-tumor effects.

resultsMET can inhibit the proliferation of LUAD cells and induce apoptosis, exerting its anticancer activity. Moreover, MET reduced the expression of CCNA2 in LUAD cells, and when the expression of CCNA2 was down-regulated, the anti-tumor cell activity of MET was promoted. In addition, MET had a good binding ability with E2F1, and MET down-regulated the expression of E2F1 in LUAD. Down-regulating the expression of E2F1 could reduce the expression of CCNA2 and enhance the inhibitory effect of MET on the proliferation of LUAD cells.

conclusionIn conclusion, our findings revealed a novel mechanism for LUAD treatment in which MET can down-regulate CCNA2 expression via E2F1 and thus exert its anti-tumor effects.

Indexed as

Adenocarcinoma of LungAntineoplastic AgentsE2F1 Transcription FactorLung NeoplasmsMetforminApoptosisCell Line, TumorCell MovementCell ProliferationDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansMolecular Docking SimulationAntineoplastic AgentsE2F1 protein, humanE2F1 Transcription FactorMetforminanti-tumor cell activity.bioinformaticsCCNA2E2F1lung adenocarcinomaMetformin

Identifiers

PMID40183277

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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.