Methylation Profiling SOCS2 in Philadelphia-Negative Myeloproliferative Neoplasm

Abstract

The Janus kinase signal transducer and activator of transcription (JAK / STAT) signalling, which is crucial in Philadelphia-negative myeloproliferative neoplasms’ (MPNs), is negatively regulated by molecules such as SOCS, CISH, and SHP1. SOCS2 methylation has been studied in MPN with conflicting results. Here we examine the methylation status of SOCS2 by specific methylation-specific polymerase chain reaction (MSP) in cell lines and 130 diagnostic prepheral blood samples from Ph-ve MPN. Furthermore, we tried to explain the mismatch of the methylation frequency by assigning the investigated MSP primers to the respective genes. Methylation was detected in normal controls using SOCS2-MSP primers in the 3 'translated exon sequence, but not with primers around the transcription start site in the 5' untranslated regions (5'UTR). SOCS2 was completely unmethylated in primary MPN samples and cell lines. In contrast, SOCS2 methylation when using MSP primers located at the 5'UTR is rare in all studies.
 In conclusion, SOCS2 methylation is rare in Ph-ve MPN. The appropriate MSP primers are important for an accurate estimate of the methylation frequency. The role of SOCS2 methylation in MPN pathogenesis requires further investigation.

Unmasking early colorectal cancer clues: in silico and in vitro investigation of downregulated IGF2, SOCS1, MLH1, and CACNA1G in SSA polyps

“…IGF2 (Insulin-like Growth Factor 2) is a gene that encodes a protein involved in cell growth and differentiation [ 33 ]. SOCS1 (Suppressor of Cytokine Signaling 1) is a gene that encodes a protein that negatively regulates cytokine signaling pathways [ 34 ]. The identification of these 4 important genes within the Weisenberger panel suggests that they may play a critical role in the molecular mechanisms underlying cancer development and could potentially serve as targets for future cancer therapies.…”