Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2020
[Effects of farnesyltransferase silencing on the migration and invasion of tongue squamous cell carcinoma].
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sheng Shan-Gui, Wang Ya-Nan, Wang Shao-Ru, Zhao Kai, Wang Yun-Ying, Xu Xiao-Na, Wang Qi-Min, Tong Lei, Chen Zheng-Gang
Аннотация
OBJECTIVE: 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.
METHODS: 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.
RESULTS: The mRNA and protein expression of FTase in the experimental group decreased compared with that in the negative control and blank control groups (P<0.05). The mRNA and protein expression of HRAS was not significantly different among the groups (P>0.05). In the experimental group, the protein expression of p-p65(S536), MMP-9, HIF-1α, and VEGF decreased (P<0.05), whereas that of p65 had no significant change (P>0.05). The migration and invasion abilities of the experimental group were inhibited significantly (P<0.05).
CONCLUSIONS: 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.
METHODS: 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.
RESULTS: The mRNA and protein expression of FTase in the experimental group decreased compared with that in the negative control and blank control groups (P<0.05). The mRNA and protein expression of HRAS was not significantly different among the groups (P>0.05). In the experimental group, the protein expression of p-p65(S536), MMP-9, HIF-1α, and VEGF decreased (P<0.05), whereas that of p65 had no significant change (P>0.05). The migration and invasion abilities of the experimental group were inhibited significantly (P<0.05).
CONCLUSIONS: 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.