No significant association between the TGFB1C-509T, T869C, and G915C polymorphisms and risk of gastric cancer was observed in overall analyses and subgroup analyses according to ethnicity.
In the subjects with ≥2 GC-relatives, TGFB1-509T/T was a risk factor for GC (OR 23.74; 95% CI 1.37-410.91), as were rural residency in childhood, alcohol consumption, spicy food ingestion, and cagA positivity.
The intrafamilial aggregation of GC might be associated with environmental factors during childhood or TGFB1-509 genetic polymorphism, or possibly H. pylori virulence.
Although many researchers have conducted association studies between TGFB1C-509T polymorphism and the risk of developing gastric cancer, the results are not uniform.
The HER-2 positive SGC-7901 secreted more transforming growth factor beta 1 (TGF-β1) and resultantly activated MMP-9 to enhance s-ICAM-1 secretion and further studies showed that phosphatidylinositol-3 kinase (PI3K)/Akt/NF-κB signaling pathway was involved in GC pathogenesis.
ASPP2 suppresses invasion and TGF-β1-induced epithelial-mesenchymal transition by inhibiting Smad7 degradation mediated by E3 ubiquitin ligase ITCH in gastric cancer.
Our evidence suggested that serum concentration of TGF-beta1 might be a novel tumor marker for GC and the polymorphisms of TGF-beta1 gene did not play a role as a determinant of serum TGF-beta1 concentration or as a genetic risk factor in the gastric carcinogenesis and progression.
EMT induced in MGC-803 cells by TGF-β1 was accompanied by S1PR1 activation, while knockdown of S1PR1 reduced response to TGF-β1, suggest that Gal-1 promotes GC invasion by activating EMT through a S1PR1-dependent mechanism.
Evaluation of Effects of TGF-β1 Inhibition on Gastric Cancer in Nude Mice by Diffusion Kurtosis Imaging and In-Line X-ray Phase Contrast Imaging With Sequential Histology.
In conclusion, these results indicated that the interaction of gastric cancer with peritoneal fibrosis and determined that TGF-β1 plays a key role in induction of peritoneal fibrosis, which in turn affected dissemination of gastric cancer.
We found that GLI-1 facilitates the EMT induced by TGF-β1 in SGC-7901 cells, which may serve as a potential target in developing the clinical treatment of gastric cancer.
Reverse transcription polymerase chain reaction (RT-PCR) was performed to detect the main components of the TGF-beta1/Smads signal pathway in human poorly differentiated GC cell line BGC-823.