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2000
Volume 25, Issue 10
  • ISSN: 1566-5240
  • E-ISSN: 1875-5666

Abstract

Objective

This study aimed to examine the molecular mechanisms involved in transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT) in human lung adenocarcinoma (LUAD) A549 cells.

Methods

Proteins were extracted from cultured human LUAD A549 cells cultured under two conditions: untreated and treated with TGF-β (5 ng/ml) for 48 hours. The expression levels of EMT-related proteins, including E-cadherin, Vimentin, and α-smooth muscle actin, were assessed using western blotting. Proteomic analysis was performed using isobaric tags for relative and absolute quantification combined with two-dimensional liquid chromatography-tandem mass spectrometry. Differentially expressed proteins were subjected to bioinformatics analysis, including functional annotation and interaction network studies.

Results

A total of 122 proteins were identified as differentially expressed between the untreated and TGF-β-treated A549 cells. Of these, 55 proteins were upregulated, while 67 were downregulated following TGF-β treatment. Bioinformatics and interaction network analyses highlighted six proteins—GAPDH, TP53, MAPK1, IGF1, SRC, and MYC—as being closely associated with the EMT in human LUAD.

Conclusion

This study provides new insights into the processes of invasion and metastasis in LUAD by examining the molecular mechanisms underlying TGF-β-induced EMT in A549 cells.

© 2025 Bentham Science Publishers
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2025-03-07
2025-12-26

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Proteomic Analysis of Molecular Mechanisms Involved in TGF-β-Induced Epithelial-Mesenchymal Transition in Human Lung Adenocarcinoma A549 Cells
Current Molecular Medicine 25, 1301 (2025); https://doi.org/10.2174/0115665240356010250304053147
/content/journals/cmm/10.2174/0115665240356010250304053147
/content/journals/cmm/10.2174/0115665240356010250304053147
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  • Article Type:     Research Article
Keyword(s): A549 cells; differential proteomics; epithelial-mesenchymal transition; lung adenocarcinoma; molecular mechanism; TGF-β

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