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Imparting epithelial to mesenchymal transition (EMT) during cellular transformation, a major driving force behind tumor progression, is one of the notorious oncogenic activities of transforming growth factor β (TGFβ); however, the secretary factors released during TGFβ-induced EMT that may have role in potentiating EMT and tumor progression are poorly known. This study was undertaken to identify such secreted protein factors from TGFβ-induced A549 cells cultured in serum-free chemically defined medium (Freestyle ) using Matrix Assisted Laser Desorption Ionization-Time of flight/Time of flight (MALDI-TOF/TOF) mass spectrometry. We identified some of the potential factors such as ESR, ANXA2, ALDH1A, TGFβ-induced protein ig-h3, and PAI-1 that were not only secreted but some were also elevated in TGFβ-induced A549 cells. Interestingly, these factors are widely reported to play crucial role in EMT induction and progression, which not only validates our findings but also opens avenues for further investigation, if upon secretion they act exogenously through certain receptors to potentiate cellular signaling involved in EMT induction and tumor progression.
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http://dx.doi.org/10.1002/bab.2121 | DOI Listing |
Chem Biodivers
September 2025
Department of Pharmaceutical Analysis, School of Pharmacy, Hebei Medical University, Shijiazhuang, People's Republic of China.
Usnic acid, a compound from Usneae Filum, has shown notable antitumor effects. Nevertheless, the mechanism of its anti-NSCLC action remains incompletely elucidated. This study used metabolomics, network pharmacology, molecular docking, and dynamics simulation to investigate usnic acid's potential mechanism on NSCLC utilizing A549 cell samples.
View Article and Find Full Text PDFCisplatin resistance significantly limits the efficacy of chemotherapy in non-small cell lung cancer, necessitating the development of new strategies to overcome this barrier. This in vitro study aimed to elucidate the mechanism by which β-Ele reverses cisplatin resistance in lung adenocarcinoma cells via the LINC00511-mediated glycolysis and Wnt/β-catenin signaling pathways. The cisplatin-resistant human lung adenocarcinoma cell line (A549/DDP), with either LINC00511 overexpression or knockdown, was established through plasmid transfection.
View Article and Find Full Text PDFCell Mol Biol (Noisy-le-grand)
September 2025
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Despite significant advancements in the treatment of non-small cell lung cancer (NSCLC) using conventional therapeutic methods, drug resistance remains a major factor contributing to disease recurrence. In this study, we aimed to explore the potential benefits of combining PI3K inhibition with Cisplatin in the context of NSCLC-derived A549 cells. Human non-small cell lung cancer A549 cells were cultured and treated with BKM120, cisplatin, or their combination.
View Article and Find Full Text PDFDrug Dev Res
September 2025
Department of Pharmaceutical Chemistry, ISF College of Pharmacy, Moga, Punjab, India.
The epidermal growth factor receptor (EGFR) is a common diver gene for lung cancer (NSCLC), which leads to an increasing death rate worldwide. This study reports the design, synthesis, and biological evaluation of triazole-clubbed pyrimidine derivatives (RDa-RDm) as potential anticancer agents. Thirteen compounds were synthesized and screened against the A549 lung cancer cell line.
View Article and Find Full Text PDFRSC Med Chem
August 2025
Department of Chemistry, National Institute of Technology Agartala Jirania-799046, West Tripura Tripura India.
The utility of bio-reductive prodrugs in cancer research has emerged as an attractive strategy. We synthesized and characterized a couple of cobalt(iii)-Schiff base complexes of general molecular formula Co(L)(L) and Co(L)(dox) , where L and L are ,-(ethane-1,2-diyl)bis(1-(pyridine-2-yl)methanimine) and 1-phenyl-1,3-butanedione, and dox = doxorubicin, as bio-reductive prodrugs. UV-vis and fluorescence spectroscopic assays confirmed the reductive release of doxorubicin from the complex in a GSH-dependent manner under physiological conditions, showing its potential for drug release.
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