Promoter hypermethylation of PTPL1, PTPN6, DAPK, p16 and 5-azacitidine inhibits growth in DLBCL.

摘要: Aberrant hypermethylation of CpG islands tumor suppressor is one the mechanisms for epigenetic loss gene function. In present study, methylation status promoter regions protein tyrosine phosphatase (PTPN) 6, DAPK, and p16 were studied using methylation-specific polymerase chain reaction (MSP) in 26 diffuse large B cell lymphoma (DLBCL) lymphomas. OCI-LY1 line, status, expression PTPL1 its reactivation by DNA demethylation was determined PCR on level western blotting. ELISA-like used to detect global measurement. Induction apoptosis 5-azacitidine analyzed Annexin V/PI staining flow cytometry. Our results show that PTPN6 region found 15.4% (4/26), DAPK 30.8% (8/26), 7.7% (2/26). Notably, we identified hypermethylated transcriptionally silenced line. The re-inducible 5-azacytidine. 5-azacytidine also inhibits proliferation decreases We can conclude from our study a higher prevalence PTPL1, PTPN6, occur DLBCL. data highlights as potential therapeutic candidate Further studies are required substantiate role marker lymphoma.