To test this hypothesis, we investigated the association of the TGF-beta1 -509C > T and 869T > C (L10P) polymorphisms and their haplotypes with the risk of lung cancer in a Korean population.
Association between single nucleotide polymorphisms of the transforming growth factor β1 gene and the risk of severe radiation esophagitis in patients with lung cancer.
However, for TGF-β1 T + 869C, subgroup analysis showed no correlation between the T + 869C polymorphism and lung cancer susceptibility in patients with NSCLC.
These results suggest that IL-10, TNF-alpha and TGF-beta1 gene polymorphisms may affect host susceptibility to lung cancer and the outcome of the patients.
Overall, no significant association was found between the TGFβ1T+869C polymorphism and lung cancer susceptibility under any genetic models in the total population (p > 0.05).
Treatment with TGF-β1 facilitated migration of human lung cancer A549 cells, which was blocked by pretreatment with ecto-nucleotidase and P2 receptor antagonists.
Kaempferol Suppresses Transforming Growth Factor-β1-Induced Epithelial-to-Mesenchymal Transition and Migration of A549 Lung Cancer Cells by Inhibiting Akt1-Mediated Phosphorylation of Smad3 at Threonine-179.
Finally, exposing A549 cells stably expressing ACE2 to DX600, an inhibitor of ACE2, recovered the sensitivity of lung cancer cells to TGF-β1-mediated induction of EMT.
The expression levels of p57(KIP2) and TGF-beta 1 were significantly associated with histological types of lung cancer (p<0.05), and the expression levels of decorin and p57(KIP2) were significantly associated with lymphatic invasion (p<0.05).
In this study, we found that sFRP1 was dramatically downregulated in transforming growth factor β1 (TGF-β1)-induced EMT in the A549 human lung cancer cell line.
Our study identified the TGFβ1/integrin β3 axis as a promising target for combination therapy to delay or overcome acquired resistance to EGFR TKIs in EGFR-mutant lung cancer.