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EP775 Differential expression of SOCS2 gene and its putative role in ovarian cancer
  1. F Al Kindi1,
  2. M Al Kalbani2,
  3. M Al Moundhri2,
  4. I Burney2 and
  5. Y Tamimi1
  1. 1Biochemistry
  2. 2Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman

Abstract

Introduction/Background Epithelial Ovarian Cancer (EOC) is the most lethal disease among gynecologic cancers. It is usually diagnosed at late stages with a poor outcome due to its asymptomatic nature. In Oman, the incidence rate for 2013 was estimated at 2.9 per 100,000. There is an urgent need to identify biomarkers for an early detection of EOC. we used chromatin immune precipitation (ChIP) to identify downstream genes regulated by the E2F5 transcription factor (TF) in ovarian cancer cell lines (MCAS and OVSAHO). Results revealed that SOCS-2 was regulated by the TF E2F5. SOCS (1–8) family have a role in JAK/STAT transcription pathway. Any disruption in this pathway may lead to many diseases such as cancers. Some of these SOCS genes found to act as biomarker for some cancers. SOCS2 was recently shown to act as an early biomarker for prostate and colorectal cancer.

The aim of this study is to explore the role of SOCS2 gene in EOC by monitoring the expression of the gene in stages variety of EOC tissues and cell lines.

Methodology We examined the expression of SOCS2 in tissues and cell lines using the quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to monitor the differential expression of SOCS2 in cancerous and normal tissues.

Results Significant down-regulation of SOCS2 was found in borderline tissues but it was not significant in other cancer stages such as benign and malignant tissues. Although all examined cell lines (MCAS, OVSAHO and 2008OV) showed a significant downregulation of the gene. SOCS2 methylation was investigated using MSP technique. It was revealed that SOCS2 is methylated in OVSAHO cell line but not in MCAS cells while cancerous tissues showed partially methylation.

Conclusion The down regulation of SOCS2 gene in EOC is not caused by methylation; other mechanisms might be involved.

Disclosure Nothing to disclose.

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