Correlation analysis showed that plasma levels of MIR4435-2HG and TGF-β1 were positively correlated only in OC patients. qPCR and western blot analysis results showed that MIR4435-2HG overexpression led to upregulation of TGF-β1 in OC cells, while TGF-β1 treatment did not significantly affect MIR4435-2HG expression.
The present study aimed to explore the mechanism underlying transforming growth factor-β (TGF‑β) 1‑mediated CSTB regulation, and to examine the function of CSTB on OC cell proliferation and apoptosis.
Results showed that exposure to TGF-β1 induced phosphorylation of SMAD2 and SMAD3 in all tested OC cell lines, but this induction was suppressed by pretreatment with LY.
Our results revealed that miR-30d functioned as a suppressor of ovarian cancer progression by decreasing Snail expression and thus blocking TGF-β1-induced EMT process, suggesting the potentiality of miR-30d analogs to be used as therapeutics for ovarian cancer.
It has been suggested that the 6A allele of the type I TGFbeta receptor (TGFbetaR1) polyalanine repeat tract polymorphism may increase susceptibility to various types of cancer including ovarian cancer.
Using the differential display method, latent transforming growth factor-beta 1 (TGF-beta 1) binding protein 1 (LTBP-1) mRNA was identified as one of the enriched mRNAs in ovarian carcinoma tissues after isolation of genes responsible for the development of ovarian cancer.
In malignant tumors, TGF beta1 was more strongly expressed in high-grade ovarian carcinomas with a cystic-papillary pattern than in tumours with a solid growth pattern.