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Title :Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells
Authors :Takachi, Takayuki
Takahashi, Masahiko
Takahashi-Yoshita, Manami
Higuchi, Masaya
Obata, Miki
Mishima, Yukio
Okuda, Shujiro
Tanaka, Yuetsu
Matsuoka, Masao
Saitoh, Akihiro
Green, Patrick L.
Fuji, Masahiro
Issue Date :Apr-2015
Abstract :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 BCL11B tumor suppressor protein. In the present study, we explored whether Tax and/or HBZ play a role in downregulating BCL11B in HTLV-1-infected T-cells. Lentiviral transduction of Tax in a human T-cell line repressed the expression of BCL11B at both the protein and mRNA levels, whereas the transduction of HBZ had little effect on the expression. Tax mutants with a decreased activity for the NF-B, CREB or PDZ protein pathways still showed a reduced expression of the BCL11B protein, thereby implicating a different function of Tax in BCL11B downregulation. In addition, the HTLV-2 Tax2 protein reduced the BCL11B protein expression in T-cells. Seven HTLV-1-infected T-cell lines, including three ATL-derived cell lines, showed reduced BCL11B mRNA 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 BCL11B protein expression in HTLV-1-infected T-cells; Tax-mediated repression of BCL11B is another mechanism that Tax uses to promote oncogenesis of HTLV-1-infected T-cells.
URL :https://doi.org/10.1111/cas.12618
Type Local :雑誌掲載論文
ISSN :1347-9032
1349-7006
Publisher :Wiley
URI :http://hdl.handle.net/20.500.12000/45872
Citation :Cancer science Vol.106 no.4 p.461 -465
Appears in Collections:Peer-reviewed Journal Articles (Faculty of Medicine)

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