Human <scp>T</scp>‐cell leukemia virus type 1 <scp>T</scp>ax oncoprotein represses the expression of the <scp>BCL</scp>11<scp>B</scp> tumor suppressor in <scp>T</scp>‐cells
書誌事項
- タイトル別名
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- Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells
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説明
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-κB, 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.
収録刊行物
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- Cancer Science
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Cancer Science 106 (4), 461-465, 2015-04
Wiley Publishing Asia Pty Ltd
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詳細情報 詳細情報について
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- CRID
- 1050001335835589632
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- NII論文ID
- 120006844098
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- ISSN
- 13497006
- 13479032
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- HANDLE
- 2433/215158
- 20.500.12000/45872
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- PubMed
- 25613934
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- 本文言語コード
- en
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- 資料種別
- journal article
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