The human T-cell leukemia virus type-1 tax oncoprotein dissociates NF-κB p65^RelA-Stathmin complexes and causes catastrophic mitotic spindle damage and genomic instability.

ABSTRACT: Genomic instability is a hallmark of many cancers; however, the molecular etiology of chromosomal dysregulation is not well understood. The human T-cell leukemia virus type-1 (HTLV-1) oncoprotein Tax activates NF-κB-signaling and induces DNA-damage and aberrant chromosomal segregation through diverse mechanisms which contribute to viral carcinogenesis. Intriguingly, Stathmin/oncoprotein-18 (Op-18) depolymerizes tubulin and interacts with the p65^RelA subunit and functions as a cofactor for NF-κB-dependent transactivation. We thus hypothesized that the dissociation of p65^RelA-Stathmin/Op-18 complexes by Tax could lead to the catastrophic destabilization of microtubule (MT) spindle fibers during mitosis and provide a novel mechanistic link between NF-κB-signaling and gen

SUBMITTER: Malu A 

PROVIDER: S-EPMC6940561 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature