口腔鳞状细胞癌表达的功能性Toll样受体3可诱导细胞凋亡并减少迁移。
Functional toll-like receptor 3 expressed by oral squamous cell carcinoma induced cell apoptosis and decreased migration.
作者信息
He Zhifeng, Huang Xiaofeng, Ni Yanhong, Shi Peihua, Wang Zhiyong, Han Wei, Hu Qingang
机构信息
Central Laboratory of Stomatology, Institute and Hospital of Stomatology, Nanjing University Medical School, Nanjing University, Nanjing, China.
Department of Oral and Maxillofacial Surgery, Institute and Hospital of Stomatology, Nanjing University Medical School, Nanjing University, Nanjing, China.
出版信息
Oral Surg Oral Med Oral Pathol Oral Radiol. 2014 Jul;118(1):92-100. doi: 10.1016/j.oooo.2014.03.012. Epub 2014 Apr 5.
OBJECTIVE
The aim of this study was to investigate the expression and function of toll-like receptor 3 (TLR3) in oral squamous cell carcinoma (OSCC).
STUDY DESIGN
We first assessed TLR3 expression in 20 cases of primary OSCC tissue. Two OSCC cell lines, SCC4 and CAL27, were used for further study. Lyophilized polyinosinic-polycytidylic acid [Poly(I:C)] was used to activate TLR3 expressed by OSCC. Changes in cytokines expression, cell viability, apoptosis, and migration in OSCC were investigated.
RESULTS
TLR3 was present in both OSCC tissue and the 2 OSCC cell lines examined. Poly(I:C) stimulated robust responses in OSCC: it upregulated cytokine expression; decreased cell viability by suppressing cell proliferation and inducing apoptosis; and decreased cell migration. Poly(I:C)-TLR3-induced OSCC cell apoptosis was caspase-3-dependent.
CONCLUSIONS
The present study indicated that TLR3 might affect OSCC development and should be considered as a potential target for future OSCC immunotherapy.
目的
本研究旨在探讨Toll样受体3（TLR3）在口腔鳞状细胞癌（OSCC）中的表达及功能。
研究设计
我们首先评估了20例原发性OSCC组织中TLR3的表达。使用两种OSCC细胞系SCC4和CAL27进行进一步研究。用冻干的聚肌苷酸-聚胞苷酸[Poly（I：C）]激活OSCC表达的TLR3。研究了OSCC中细胞因子表达、细胞活力、凋亡和迁移的变化。
结果
在所检测的OSCC组织和两种OSCC细胞系中均存在TLR3。Poly（I：C）在OSCC中引发了强烈反应：它上调了细胞因子表达；通过抑制细胞增殖和诱导凋亡降低细胞活力；并减少细胞迁移。Poly（I：C）-TLR3诱导的OSCC细胞凋亡依赖于半胱天冬酶-3。
结论
本研究表明TLR3可能影响OSCC的发展，应被视为未来OSCC免疫治疗的潜在靶点。
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