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OBJECTIVE: This study aimed to explore the effects of silencing isoprenylcysteine carboxyl methyltransferase (Icmt) through small interfering RNA (siRNA) interference on the proliferation and apoptosis of tongue squamous cell carcinoma (TSCC). METHODS: Three siRNA were designed and constructed for the Icmt gene sequence and were then transfected into TSCC cells CAL-27 and SCC-4 to silence Icmt expression. The tested cells were divided as follows: RNA interference groups Icmt-siRNA-1, Icmt-siRNA-2, and Icmt-siRNA-3, negative control group, and blank control group. The transfection efficiency of siRNA was detected by the fluorescent group Cy3-labeled siRNA, and the expression of Icmt mRNA was screened by quantitive real-time polymerase chain reaction (qRT-PCR) selected the experimental group for subsequent experiments. The expression of Icmt, RhoA, Cyclin D1, p21, extracellular regulated protein kinases (ERK), and phospho-extracellular regulated protein kinases (p-ERK) were analyzed by Western blot. The proliferation abilities of TSCC cells were determined by cell counting kit-8 assay. The change in apoptosis was detected by AnnexinV-APC/propidium staining (PI) assay. Cell-cycle analysis was conducted by flow cytometry. RESULTS: The expression of Icmt mRNA and protein in TSCC cells significantly decreased after Icmt-siRNA transfection (P0.05), but the expression of RhoA membrane protein decreased compared with the negative control group and blank control groups (P0.05). However, the phosphorylation level of ERK was significantly reduced (P

To investigate the effect of human bone marrow mesenchymal stem cells (hBM-MSCs) on invasion of tongue squamous cell carcinoma cell line Cal-27 and its mechanism.hBM-MSCs and Cal-27 were cultured respectively, and the morphology of the cells was observed under an inverted microscope. The co-cultured Cal-27 cells were obtained by co-culture of hBM-MSCs and Cal-27. The migration area of Cal-27 was observed by scratch test;transwell migration and invasion experiments were performed to observe migration and invasion of Cal-27, and a bar graph was then drawn. Fluorescence quantitative PCR was used to observe the effect of hBM-MSCs on gene expression of the tumor markers E-cadherin, twist, slug, snail, MMP-2 and MMP-9. Western blot was used to observe the effect of hBM-MSCs on protein expression of MMP-2 and MMP-9, related to the invasion of Cal-27. SPSS 19.0 software package was used for statistical analysis of the data.Under the influence of hBM-MSCs, the invasion of Cal-27 was promoted, accompanied by down-regulation of E-cadherin, up-regulation of twist, slug, snail, MMP-2, MMP-9 and up-regulation of MMP-2 and MMP-9 expression.hBM-MSCs can promote invasion of Cal-27 cells, which may be related to up-regulation of the expression of tumor markers related to invasion of Cal-27 cells.

This study aimed to explore the effects of silencing farnesyltransferase (FTase) on the migration and invasion of tongue squamous cell carcinoma (TSCC) through RNA interference.TSCC cells (CAL27 and SCC-4) were cultured in vitro and then transfected with siRNA to silence FTase expression. The tested cells were categorized as follows: experimental group (three RNA interference groups), negative control group, and blank control group. mRNA expression of FTase and HRAS in each group was analyzed by quantitative real-time polymerase chain reaction. On the basis of FTase mRNA expression, the optimum interference group (highest silencing efficiency) was selected as the experimental group for further study. The protein expression of FTase, HRAS, p65, p-p65(S536), matrix metalloprotein-9 (MMP-9), hypoxia inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) was analyzed by Western blot. The invasion and migration abilities of TSCC cells were determined by Transwell invasion assay and cell wound healing assay.The mRNA and protein expression of FTase in the experimental group decreased compared with that in the negative control and blank control groups (P0.05). The mRNA and protein expression of HRAS was not significantly different among the groups (P0.05). In the experimental group, the protein expression of p-p65(S536), MMP-9, HIF-1α, and VEGF decreased (P0.05), whereas that of p65 had no significant change (P0.05). The migration and invasion abilities of the experimental group were inhibited significantly (P0.05).Silencing FTase in vitro could effectively downregulate its expression in TSCC cell lines and reduce the migration and invasion abilities to a certain extent. FTase could be a new gene therapy target of TSCC, and this research provided a new idea for the clinical treatment of TSCC.目的 通过RNA干扰沉默法尼基转移酶（FTase），探讨沉默FTase对舌鳞状细胞癌迁移和侵袭的影响及其相关机制。方法 针对FTase设计并构建3条小干扰RNA（siRNA），转染人舌鳞状细胞癌CAL27和SCC-4细胞（实验组），同时设置阴性对照组（转染NC-siRNA）和空白对照组（不转染siRNA）。应用实时荧光定量PCR检测各组细胞FTase、HRAS的mRNA表达，根据FTase mRNA的表达量，选取沉默效率最高的FTase-siRNA转染组作为进一步研究的实验组。蛋白质免疫印迹法检测各组细胞FTase、HRAS、p65、p-p65(S536)、基质金属蛋白酶9（MMP-9）、低氧诱导因子1α（HIF-1α）、血管内皮生长因子（VEGF）的蛋白表达，Transwell侵袭实验和细胞划痕实验检测各组细胞的侵袭和迁移能力。结果 与阴性对照组和空白对照组相比，实验组FTase的mRNA和蛋白表达下降（P 0.05），HRAS的mRNA和蛋白表达无明显变化（P0.05），p-p65(S536)、MMP-9、HIF-1α、VEGF蛋白表达下降（P0.05），p65蛋白表达无明显变化（P0.05）；实验组的细胞侵袭和迁移能力降低（P0.05）。结论 体外沉默舌鳞状细胞癌细胞FTase，可以抑制细胞体外迁移和侵袭能力，为FTase可能作为舌癌治疗的分子靶点提供了一定的理论和实验依据.