Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology · 2004
[The inhibitory effect of human endostatin gene on tumor growth of tongue squamous cell carcinoma].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание 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.
Pan Chao-bin, Huang Hong-zhang, Wang Jian-guang, Hou Jin-song, Li Hai-gang
Аннотация
OBJECTIVE: To investigate the expression of transfected human endostatin (hES) gene in tongue squamous cell carcinoma (TSCC) and its inhibitory effects on the growth of tumor cells in vivo.
METHODS: Lipofectamine-mediated hES gene was transferred into Tca8113 cells, selected with Blasticidin S; The stable transfected cells were inoculated in BALB/c mice, and then the growth of xenografts was observed. The hES and vascular endothelial growth factor (VEGF) protein expression of xenografts was detected by S-P immuno-histochemical assay. We also detected the microvessel density (MVD) of xenografts with Weidern's method and apoptotic index of the tumor cells by flow cytometry (FCM).
RESULTS: The hES protein expression of xenografts in experimental group was significantly higher than that in control group (P < 0.01), while the expression of VEGF protein was on the other way round (P < 0.01). MVD counting of xenografts in experimental group was lower than that in control group (P < 0.01). The mean apoptotic level of the tumor cells in control group was also lower than in experimental group (P < 0.01). In addition, the inhibitory rate to growth of xenografts induced by hES transfection was 78.9%.
CONCLUSIONS: hES gene can be transferred into TSCC cells and then induce corresponding protein expression efficiently in xenograft model, resulting in significantly inhibitory effects on the xenografts in vivo.
METHODS: Lipofectamine-mediated hES gene was transferred into Tca8113 cells, selected with Blasticidin S; The stable transfected cells were inoculated in BALB/c mice, and then the growth of xenografts was observed. The hES and vascular endothelial growth factor (VEGF) protein expression of xenografts was detected by S-P immuno-histochemical assay. We also detected the microvessel density (MVD) of xenografts with Weidern's method and apoptotic index of the tumor cells by flow cytometry (FCM).
RESULTS: The hES protein expression of xenografts in experimental group was significantly higher than that in control group (P < 0.01), while the expression of VEGF protein was on the other way round (P < 0.01). MVD counting of xenografts in experimental group was lower than that in control group (P < 0.01). The mean apoptotic level of the tumor cells in control group was also lower than in experimental group (P < 0.01). In addition, the inhibitory rate to growth of xenografts induced by hES transfection was 78.9%.
CONCLUSIONS: hES gene can be transferred into TSCC cells and then induce corresponding protein expression efficiently in xenograft model, resulting in significantly inhibitory effects on the xenografts in vivo.