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.
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 novelty of the study also resides with the fact in the expression of different lineage-specific markers, like CD31, CD45, and CD117 along with CD44 in the TGFβ1-induced epithelial ovarian cancer spheroids.
The effect of TGF-β signaling on STAT1 activation was examined in EOC and non-tumorous HOSEpiC cells treated with TGF-β1 in the presence or absence of the inhibitor of TGF-β type I receptor.
Besides, we noticed that the high pre-operative concentration of TGF-β1 could distinguish all EOC patients (independently of FIGO classification) for whom optimal or sub-optimal surgery would be applied.
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.
ZEB2 and TGF-β1 may promote EOC progression, and FIGO stage, TGF-β1 expression, postoperative start time of chemotherapy, and treatment course may be associated with the prognosis of EOC.
These data indicate that hAECs endow potential anticancer properties on epithelial ovarian cancer in vivo and in vitro which is partially mediated by hAEC‑secreted TGF‑β1-induced cell cycle arrest.
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.
Endometriosis and EOC cells manifested significantly higher mRNA levels of TGF-β1, COX-2, VEGF, ER-1α, AR, and aromatase, while they expressed significantly lower mRNA levels of PR.
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.