Twist2 regulates CD7 expression and galectin-1-induced apoptosis in mature T-cells |
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Authors: | Han Seok Koh Changjin Lee Kwang Soo Lee Eun Jung Park Rho H Seong Seokmann Hong Sung Ho Jeon |
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Institution: | (1) Neurologische Universitätsklinik Wien, Austria;(2) Abteilung Spez. Neuropathologie am Neurologischen Institut der Universität Wien, Austria;(3) Ludwig Boltzmann-Institut für Leukämieforschung und Hämatologie am Hanusch-Krankenhaus Wien, Austria; |
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Abstract: | In the periphery, a galectin-1 receptor, CD7, plays crucial roles in galectin-1-mediated apoptosis of activated T-cells as
well as progression of T-lymphoma. Previously, we demonstrated that NF-κB downregulated CD7 gene expression through the p38
MAPK pathway in developing immature thymocytes. However, its regulatory pathway is not well understood in functional mature
T-cells. Here, we show that CD7 expression was downregulated by Twist2 in Jurkat cells, a human acute T-cell lymphoma cell
line, and in EL4 cells, a mature murine T-cell lymphoma cell line. Furthermore, ectopic expression of Twist2 in Jurkat cells
reduced galectin-1-induced apoptosis. While full-length Twist2 decreased CD7 promoter activity, a C-terminal deletion form
of Twist2 reversed its inhibition, suggesting an important role of the C-terminus in CD7 regulation. In addition, CD7 expression
was enhanced by histone deacetylase inhibitors such as trichostatin A and sodium butyrate, which indicates that Twist2 might
be one of candidate factors involved in histone deacetylation. Based on these results, we conclude that upregulation of Twist2
increases the resistance to galectin-1-mediated-apoptosis, which may have significant implications for the progression of
some T-cells into tumors such as Sezary cells. |
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