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.
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.
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.
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.
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.
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.
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.