NF-κB and MicroRNA Deregulation Mediated by HTLV-1 Tax and HBZ

Stefania Fochi; Vincenzo Ciminale; Elisabetta Trabetti; Umberto Bertazzoni; Donna M D'Agostino; Donato Zipeto; Maria Grazia Romanelli

doi:10.3390/pathogens8040290

NF-κB and MicroRNA Deregulation Mediated by HTLV-1 Tax and HBZ

Pathogens. 2019 Dec 10;8(4):290. doi: 10.3390/pathogens8040290.

Authors

Stefania Fochi¹, Vincenzo Ciminale^{2

3}, Elisabetta Trabetti¹, Umberto Bertazzoni¹, Donna M D'Agostino⁴, Donato Zipeto¹, Maria Grazia Romanelli¹

Affiliations

¹ Department of Neurosciences, Biomedicine and Movement Sciences, Section of Biology and Genetics, University of Verona, 37134 Verona, Italy.
² Department of Surgery, Oncology and Gastroenterology, University of Padua, 35128 Padua, Italy.
³ Veneto Institute of Oncology IOV-IRCCS, 35128 Padua, Italy.
⁴ Department of Biomedical Sciences, University of Padua, 35131 Padua, Italy.

Abstract

The risk of developing adult T-cell leukemia/lymphoma (ATLL) in individuals infected with human T-cell lymphotropic virus 1 (HTLV-1) is about 3-5%. The mechanisms by which the virus triggers this aggressive cancer are still an area of intensive investigation. The viral protein Tax-1, together with additional regulatory proteins, in particular HTLV-1 basic leucine zipper factor (HBZ), are recognized as relevant viral factors required for both viral replication and transformation of infected cells. Tax-1 deregulates several cellular pathways affecting the cell cycle, survival, and proliferation. The effects of Tax-1 on the NF-κB pathway have been thoroughly studied. Recent studies also revealed the impact of Tax-1 and HBZ on microRNA expression. In this review, we summarize the recent progress in understanding the contribution of HTLV-1 Tax- and HBZ-mediated deregulation of NF-κB and the microRNA regulatory network to HTLV-1 pathogenesis.

Keywords: HBZ; HTLV-1; NF-κB; Tax; miRNA.

Publication types

Review