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Human T cell leukemia virus type 1 (HTLV-1) Tax-induced persistent activationof the NF-κB pathway is perceived as the primary cause of adult T cell leukemia(ATL), an aggressive leukemia caused by HTLV-1. Although elevated oncoproteinBcl-3 levels are found in many HTLV-1-infected T cell lines and ATL cells, therole of Bcl-3 in the malignant progression caused by HTLV-1 retrovirus remainspoorly understood. We confirmed, in the present study, that the Tax-induced NF-κBactivation involves the regulation of Bcl-3. Both knockdown and overexpressionof Bcl-3 inhibit the Tax-induced NF-κB activation. Similarly, excessive Bcl-3inhibits the NF-κB/DNA binding activity and significantly decreases Tax-inducedp65 nuclear translocation. The present results demonstrate the pleiotropic rolesof Bcl-3 in Tax-induced NF-κB activation and indicate that a balance in the aberrantBcl-3 expression may be established to play an important role in the maintenanceof proliferation and inhibition of apoptosis in HTLV-1-infected and ATL cells.

Bcl-3 suppresses Tax-induced NF-κB activation through p65 nuclear translocation blockage in HTLV-1-infected cells