Evidence map›Paper›PMID 41388437›Full record

ArticleEuropean journal of medical research2025

MYBL2 regulates the expression of CENPF in lung adenocarcinoma and promotes tumor development and metastasis through AKT pathway activation.

Yan Liu, Feng Yu, Jiuyang Jiang, Hongmei Ma

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Article in European journal of medical research, 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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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Yan LiuTest Room of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, 199 Dongdazhi Street, Nangang District, Harbin, 150001, Heilongjiang, China. 810437@hrbmu.edu.cn.
Feng YuTest Room of Clinical Laboratory, The First Affiliated Hospital of Harbin Medical University, 199 Dongdazhi Street, Nangang District, Harbin, 150001, Heilongjiang, China.
Jiuyang JiangDepartment of Thoracic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Hongmei MaTest Room of Clinical Laboratory, Xiamen Hospital of Traditional Chinese Medicine, Xiamen, 361000, China. Mahm77lw@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesLung adenocarcinoma (LUAD) is a major global health burden with high mortality. Elevated expression of MYBL2 and CENPF is correlated with unfavorable clinical outcomes in LUAD. However, the relationship between MYBL2 and CENPF and the downstream signaling pathways of MYBL2 and CENPF in LUAD remains elusive.

methodsWe investigated MYBL2 and CENPF expression in TCGA data and clinical LUAD samples, identifying a significant correlation. Functional studies in A549 cells demonstrated that MYBL2 acts upstream of CENPF, promoting tumor proliferation and migration. This oncogenic effect was mediated through AKT signaling, as AKT inhibition phenocopied the suppressive effects of CENPF knockdown.

resultsAnalysis of TCGA data and clinical specimens confirmed significant upregulation of MYBL2 and CENPF in LUAD compared to normal tissues. Their expression correlated positively with advanced disease stage and poorer prognosis across diverse patient subgroups. Functional studies demonstrated that MYBL2 acts upstream of CENPF, as its overexpression elevated CENPF levels, while its knockdown reduced them. CENPF depletion markedly attenuated LUAD cell proliferation and migration. Mechanistically, both MYBL2 overexpression and CENPF knockdown modulated AKT pathway activation, as evidenced by altered phosphorylation levels. Accordingly, pharmacological inhibition of AKT with GDC-0068 recapitulated the anti-tumor effects observed with CENPF knockdown.

conclusionsThe expression of MYBL2 and CENPF in lung adenocarcinoma increases with LUAD progression. MYBL2 regulates the expression of CENPF in LUAD, and the elevated CENPF promotes the proliferation and migration of LUAD cells. Both MYBL2 and CENPF regulate the proliferation and migration of LUAD through AKT pathway activation.

Indexed as

Adenocarcinoma of LungCell Cycle ProteinsLung NeoplasmsProto-Oncogene Proteins c-aktTrans-ActivatorsA549 CellsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisPrognosisSignal TransductionCell Cycle ProteinsProto-Oncogene Proteins c-aktTrans-ActivatorsCENPFLung adenocarcinomaMYBL2p-AKTTumor metastasis

Identifiers

PMID41388437
PMCPMC12817451

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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.