Objectives The SOCS3 gene is a key regulator for JAK/STAT pathway, responsible for inflammation and proliferation response, was found to be regulated by E2F5 and its down regulation seems to have a role in the pathogenesis of different tumors including gastric and pancreatic cancers.
Our aim to investigate the involvement of SOCS3 gene in EOC by monitoring its expression in ovarian cancer cell lines and EOC tissue samples, then to compare results to normal ovarian tissue samples. We also examine methylation status of both, ovarian cell lines and ovarian tissue specimen.
Methods Real time qPCR was used to assess gene expression using Taq Man gene expression assay. Five cell lines (MCAS, OVSAHO, OV 2008, A2780s and A2780cp) and 19 tissue samples with different histopathology types (6 normal, 4 benign, 5 borderlines and 4 high grade serous) were examined. Methylation status analysis was performed by methylation specific PCR
Results OVSAHO, OV2008 and A2780s cell lines showed down regulation of SOCS3 expression when compared to normal. Benign, borderline and high grades samples, displayed also significant down regulation of SOCS3 expression. Analysis of methylation pattern showed no hyper-methylation in both cell lines and tissues.
Conclusions Down regulation of SOCS3 gene expression was detected in ovarian cancer cell lines and EOC tissue samples, suggesting a putative role of SOCS3 in the pathogenesis of EOC. Other epigenetics mechanisms such as micro-RNAs are involved in the regulation of SOCS3 expression in addition to hyper-methylation and therefore, further study is needed to uncover these mechanisms.
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.