Growth inhibition of Tax-activated human Jurkat leukemia T cells by all-trans retinoic acid requires JNK-1 inhibition

摘要: Retinoids, including vitamin A (retinol) and its analogues, are critical for a variety of biological functions. In this study, we report that all-trans retinoic acid (ATRA) decreases Jun N-terminal kinase 1 (JNK-1) activity, antagonizing the effect Tax protein in Jurkat leukemia T cells transiently transfected expressing Tax protein. The Tax protein is one products human T-cell virus type 1 (HTLV-1) which etiologic agent adult (ATL), an aggressive neoplasia CD4+ T cells. decrease JNK-1 activity was followed by marked expression interleukin (IL)-2 weak increase interferon (IFN)-γ Jurkat cells treated with ATRA dose-dependent manner, suggesting correlation between However, levels IL-4 IL-10 were enhanced cells Tax, compared untransfected cells, but not affected following treatment. transfection studies using luciferase reporter construct IL-2 promoter or tandem repeat AP-1 NF-κB, inhibitory on confirmed at transcriptional level. NF-κB only marginal. addition, our data demonstrated constitutively activated protein, required Tax-induced proliferation cells.