Evidence map›Paper›PMID 39844538›Full record

ArticleCurrent medicinal chemistry2025

SQSTM1/p62 Mediates the Effects of CPNE3 on the Epithelialmesenchymal Transition and Migration Inhibition of Lung Adenocarcinoma Cells.

Yanping Li, You Li, Liming Xu, Guangming Yang, Huansi Zhou, Mingjing Jin, Kai Yu, Chunhua Lu

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Article in Current medicinal chemistry, 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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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yanping LiGuangxi International Zhuang Medicine Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530201, China.
You LiDepartment of Biotechnology, College of Life Science and Technology, Guangxi University, Nanning, 530004, China.
Liming XuDepartment of Biotechnology, College of Life Science and Technology, Guangxi University, Nanning, 530004, China.
Guangming YangDepartment of Biotechnology, College of Life Science and Technology, Guangxi University, Nanning, 530004, China.
Huansi ZhouGuangxi International Zhuang Medicine Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530201, China.
Mingjing JinGuangxi International Zhuang Medicine Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530201, China.
Kai YuCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, China.ORCID 0000-0001-5338-3437
Chunhua LuMedical Experimental Center, The First People's Hospital of Nanning, The Fifth Affiliated Hospital of Guangxi Medical University, Nanning, 530022, China.

Funding

Guangxi University of Chinese Medicine PhD Start-up Fund Project 2020BS034Natural Science Foundation of Guangxi Province 2018GXNSFDA050009Scientific Research Start-up Fund Project for Talent Introduction of Guangxi International Zhuang Medicine Hospital GZ2021RC016
6 · The paper itself

Abstract

introductionCopine-3 (CPNE3) is a conservative calcium-dependent phospholipid- binding protein belonging to the copines protein family. CPNE3 has been implicated in the development and progression of several diseases, including cancer.

methodsHerein, we investigated the molecular mechanisms through which CPNE3 regulates the migration of lung adenocarcinoma (LUAD) cells in vitro. Western blotting and immunohistochemical assays showed that CPNE3 is widely distributed in LUAD tissues and cell lines and that CPNE3 downregulation promotes the migration of human LUAD A549 cells.

resultsStable isotope labelling with amino acids in cell culture, which is a quantitative proteomics approach coupled with bioinformatic analyses, revealed that CPNE3 regulates SQSTM1/p62 and vimentin expression, indicating that CPNE3 may mediate epithelial- mesenchymal transition (EMT). CPNE3 silencing by siRNA upregulated vimentin levels but downregulated E-cadherin levels in the A549 cells.

conclusionFurthermore, SQSTM1/p62 knockdown enhanced migratory ability and EMT progression in CPNE3-silenced A549 cells. Overall, CPNE3 knockdown was found to promote EMT by inhibiting SQSTM1/p62 signalling and facilitating cell migration. Our findings highlight the role of CPNE3 as a tumour suppressor, providing deeper insights into its tumour-suppressive roles in LUAD.

Indexed as

Adenocarcinoma of LungEpithelial-Mesenchymal TransitionLung NeoplasmsSequestosome-1 ProteinA549 CellsCell MovementHumansVimentinSequestosome-1 ProteinSQSTM1 protein, humanVimentinCPNE3EMTlung adenocarcinomaSILACSQSTM1/p62systematic screening.

Identifiers

PMID39844538

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