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Human T‐cell leukemia virus type 1 ( HTLV ‐1) is the etiological agent of adult T cell leukemia ( ATL ), which is an aggressive form of T‐cell malignancy.  HTLV ‐1 oncoproteins, Tax and  HBZ , play crucial roles in the immortalization of T‐cells and/or leukemogenesis by dysregulating the cellular functions in the host. Recent studies show that  HTLV ‐1‐infected T‐cells have reduced expression of the  BCL 11B tumor suppressor protein. In the present study, we explored whether Tax and/or  HBZ  play a role in downregulating  BCL 11 B  in  HTLV ‐1‐infected T‐cells. Lentiviral transduction of Tax in a human T‐cell line repressed the expression of  BCL 11 B  at both the protein and m RNA  levels, whereas the transduction of  HBZ  had little effect on the expression. Tax mutants with a decreased activity for the  NF ‐κ B ,  CREB  or  PDZ  protein pathways still showed a reduced expression of the  BCL 11 B  protein, thereby implicating a different function of Tax in  BCL 11 B  downregulation. In addition, the  HTLV ‐2 Tax2 protein reduced the  BCL 11 B  protein expression in T‐cells. Seven  HTLV ‐1‐infected T‐cell lines, including three  ATL ‐derived cell lines, showed reduced  BCL 11 B  m RNA  and protein expression relative to an uninfected T‐cell line, and the greatest reductions were in the cells expressing Tax. Collectively, these results indicate that Tax is responsible for suppressing  BCL 11 B  protein expression in  HTLV ‐1‐infected T‐cells; Tax‐mediated repression of  BCL 11 B  is another mechanism that Tax uses to promote oncogenesis of  HTLV ‐1‐infected T‐cells.

Human T ‐cell leukemia virus type 1 T ax oncoprotein represses the expression of the BCL 11 B tumor suppressor in T ‐cells