In conclusion, our study demonstrated that OA inhibits the generation of Tregs in lung cancer environment by inhibiting the T cells' response to TGF-β1 and decreasing the secretion of TGF-β1 in lung cancer cells via NF-κB signaling.
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.
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).
The results show that the <i>TGFβ-EMT</i> signature successfully discriminated lung cancer cell lines capable of undergoing EMT in response to TGFβ-1 and predicts MFS in lung adenocarcinomas.
Here, we focused on lung cancer and demonstrated that TGF-β1 induced the phosphorylation of Smad3 (p-Smad3), upregulation of Snail, a fibroblast-like morphology, and downregulation of E-cadherin as well as upregulation of vimentin in lung cancer cell lines.
In cervical, gastric, colorectal, breast, and lung cancer, the cause of this failure is the inadequate expression of inducible nitric oxide synthase (iNOS), resulting from the inhibition of iNOS expression by TGF-beta1 at the mRNA level.
We hypothesized that in patients with lung cancer treated with radiation therapy (RT), TGF-β1 levels may correlate with the percentages of CD4<sup>+</sup> T cells, CD8<sup>+</sup> T cells, and the CD4<sup>+</sup>/CD8<sup>+</sup> T cell ratio in peripheral blood.
Here, we identified that SPARC/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) is a novel transforming growth factor-β1 (TGF-β) target gene that regulates lung cancer cell EMT.
Treatment with TGF-β1 facilitated migration of human lung cancer A549 cells, which was blocked by pretreatment with ecto-nucleotidase and P2 receptor antagonists.
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.
In conclusion, these results suggested that AA may inhibit TGF-β1-induced EMT in lung cancer through increased expression of E-cadherin, and inhibition of Snail, N-cadherin and vimentin expression.
Here, we report that neuropilin (NRP)-2, the high-affinity receptor for SEMA3F and a coreceptor for certain growth factors, is upregulated during TGF-β1-driven EMT in lung cancer cells.
Association between single nucleotide polymorphisms of the transforming growth factor β1 gene and the risk of severe radiation esophagitis in patients with lung cancer.
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.
SIGNIFICANCE: This study provides new mechanistic insight of the interaction between HTRA3 and TGFβ in lung cancer by illustrating that HTRA3 is a novel mediator acting as a suppressor of TGFβ1-related oncogenic effects.