中文摘要：

地岬相当或相同的事物基因家庭成员 A (RhoA ) 作为肿瘤的一个批评管理者被识别了好攻击的行为。在 thisstudy，我们在位于有鳞的细胞 carcinomaof 舌头(TSCC ) 的生长，移植，和侵略下面的机制估计了 RhoA 的角色。TSCC 房间线 SCC-4 和 CAL27 击倒的稳定的 RhoA 用 Lentiviral transfection 被完成。房间移植，侵略，和房间增长上的 RhoA 弄空的 Theeffects 是坚定的。TSCC 房间线上的可能的位于决定 Galectin-3 (Gal-3 ) 的表示下面 mechanismof RhoA 弄空被也评估，在 vivo 的 -catenin, andmatrix metalloproteinase-9 (MMP-9 ) 。同时， TSCC 生长的内在的机制被 cyclin D1/2 的分析学习， p21 ^CIP1/WAF1 , 和 p27 ^Kip1 蛋白质层次。Immunohistochemical 评价被执行进一步证明 Gal-3 和 -catenin expression.We 的改变发现了那，在与在舌头的人的 TSCC 房间注射的老鼠， RhoA 层次与在正常纸巾的那些相比在主要肿瘤和 metastasizedlymph 节点是更高的。RhoA 的 Silencing 显著地减少了肿瘤生长， Gal-3 的 decreasedthe 层次， -catenin, MMP-9，和 cyclin D1/2，并且增加了 p21 ^CIP1/WAF1 和 p27 ^Kip1 。在 vitro， RhoA 击倒也导致了房间移植，侵略，和增长的抑制。我们的数据建议 RhoA 由通过分别地通过房间周期规定表明小径 andcell 增长的 Wnt/-catenin 调整房间移植和侵略在 TSCC 前进起 asignificant 作用。RhoA 可能是 TSCC 的一个新奇治疗学的目标。

英文摘要：

Ras homolog gene family member A （RhoA） has been iden- tified as a critical regulator of tumor aggressive behavior. In this study, we assessed the role of RhoA in the mechan- isms underlying growth, migration, and invasion of squa- mous cell carcinoma of tongue （TSCC）. Stable RhoA knockdown of TSCC cell lines SCC-4 and CAL27 were achieved using Lentiviral transfection. The effects of RhoA depletion on cell migration, invasion, and cell proliferation were determined. The possible underlying mechanism of RhoA depletion on TSCC cell line was also evaluated by determining the expression of Galectin-3 （Gal-3）, β-catenin, and matrix metalloproteinase-9 （MMP-9） in vivo. Meanwhile, the underlying mechanism of TSCC growth was studied by analysis of cyclin D1/2, p21clel/WArl, and p27 kiap 1 protein levels. Immunohistochemical assess- ments were performed to further prove the alteration of Gal-3 and β-catenin expression. We found that, in mice injected with human TSCC cells in the tongue, RhoA levels were higher in primary tumors and metastasized lymph nodes compared with those in the normal tissues. Silencing of RhoA significantly reduced the tumor growth, decreased the levels of Gai-3, β-catenin, MMP-9, and cyclin D1/2, and increased the levels of p21 CIPI/WAFI and p27Kiap 1. In vitro, RhoA knockdown also led to inhibition of cell migration, in- vasion, and proliferation. Our data suggest that RhoA plays a significant role in TSCC progression by regulating cell migra- tion and invasion through Wnt/β-catenin signaling pathway and cell proliferation through cell cycle regulation, respecti- vely. RhoA might be a novel therapeutic target of TSCC.