The Role of TLE1 in Synovial Sarcoma

被引:27
|
作者
Seo, Sung Wook [2 ]
Lee, Hyewon [2 ]
Lee, Hyun-Il [2 ]
Kim, Han-Soo [1 ]
机构
[1] Seoul Natl Univ, Dept Orthopaed Surg, Seoul 110744, South Korea
[2] Sungkyunkwan Univ, Dept Orthopaed Surg, Samsung Med Ctr, Seoul 135710, South Korea
关键词
synovial sarcoma; doxorubicin; TLE1; siRNA; apoptosis; WNT SIGNALING PATHWAY; GENE-EXPRESSION; CELL-LINE; APOPTOSIS; PROTEIN; PROLIFERATION; DIFFERENTIATION; ASSOCIATION; INHIBITION; PROFILES;
D O I
10.1002/jor.21318
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
The treatment outcome of synovial sarcoma is poor owing to its resistance to radiation and chemotherapy. The Transducin-like Enhancer of Split 1 (TLE1) is a co-repressor that involves many signaling pathways like cell survival, hematopoiesis and differentiation. Although TLE1 is uniquely expressed in synovial sarcomas, the biological role of TLE1 is not completely understood. This study evaluated the function of TLE1 in synovial sarcomas using knock-down of TLE1, and examined whether the inhibition of TLE1 suppresses the proliferation of synovial sarcomas and enhances the cytotoxicity caused by doxorubicin (doxo). The over-expression of TLE1 was first confirmed in synovial sarcoma cells (HS-SYII). When the HS-SYII cells and normal fibroblast were transiently transfected with TLE1 siRNA, the MTT assay revealed growth inhibition in the HS-SY-11 cells but not in the normal fibroblast. TLE1 silencing also potentiated the cytotoxic effects of doxo against HS-SYII cells. This effect of TLE1 silencing was attributed mainly to the induction of apoptosis. Subsequent analysis revealed that Bcl-2 is a possible downstream target of TLE1 signaling. This study demonstrated that TLE1 is a critical factor for the survival of synovial sarcomas. Overall, the inhibition of TLE1 affects cell proliferation and the apoptosis pathway by suppressing the expression of Bcl-2. (C) 2011 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29: 1131-1136, 2011
引用
收藏
页码:1131 / 1136
页数:6
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