HIV-1 Transactivator of Transcription (Tat) Co-operates With AP-1 Factors to Enhance c-MYC Transcription

• DOI: 10.3389/fcell.2021.693706
• Publication Date: 2021-06-30T05:44:24Z
• Authors: Leonardo Alves de...; Lungile Mapekula; Nontlantla Mdletshe; Dharshnee Chetty; Shaheen Mowla
• Keywords: Chromatin immunoprecipitation; Pathogenesis; JUNB

HIV-1 infection often leads to the development of co-morbidities including cancer. Burkitt lymphoma (BL) is one most over-represented non-Hodgkin among HIV-infected individuals, and displays a highly aggressive phenotype in this population group, with comparatively poorer outcomes, despite these patients being on anti-retroviral therapy. Accumulating evidence indicates that molecular pathogenesis HIV-associated malignancies unique, components virus playing an active role driving oncogenesis, order improve patient prognosis treatment, better understanding disease pathobiology progression needed. In study, we found Tat be localized within tumor cells BL patients, enhanced expression oncogenic c-MYC cells. Using luciferase reporter assays show enhances gene promoter activity partially mediated via two AP-1 binding elements located at positions -1128 -1375 bp, as revealed by mutagenesis experiments. We further demonstrate, using pull-down assays, can exist protein complex factor JunB, bind sites promoter, shown vivo chromatin immunoprecipitation assays. Therefore, findings infiltrates B-cells, where it enhance factors, which contributes toward more observed patients.