Figure 7From: HIV-1 Tat induces DNMT over-expression through microRNA dysregulation in HIV-related non Hodgkin lymphomasMethylation analysis of DNMT-dependent miRNAs and cell cycle regulatory genes in Tat-positive vs. Tat-negative cells and primary tumors. Methylation analysis of INK4/p16 (a) and TP53 (b) in HIV-positive and -negative primary tumors. M indicates the product using the methyled primers, U indicates the product using the unmethyled primers. Amplification of INK4/p16 resulted in a band lower than 200Â bp, whereas the specific product for TP53 was about 100Â bp. The specific product for INK4/p16 was obtained only using unmethyled primers in HIV-negative samples, whereas only methyled primers resulted in a INK4/p16 product in HIV-positive tumors, which is indicative of INK4/p16 methylation in HIV-positive tumors. No differences were observed for TP53 between HIV-negative and HIV-positive tumors, as the amplified product was obtained only using unmethyled primers, indicating that no methylation is detectable for TP53 in neither of the two tumor types. Arrows indicate the presence of specific products for both genes. (c) IHC for p16 in HIV-positive tumors; (d) Sequence analysis of hsa-miR-148a in HIV-positive and HIV-negative primary tumors. Arrows indicate the methyled C that are not converted to U in HIV-positive tumors.Back to article page