The inhibitory effect of human endostatin gene on tumor growth of tongue squamous cell carcinoma.
- Author:
Chao-bin PAN
1
;
Hong-zhang HUANG
;
Jian-guang WANG
;
Jin-song HOU
;
Hai-gang LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Carcinoma, Squamous Cell; blood supply; genetics; prevention & control; Endostatins; biosynthesis; genetics; Female; Genetic Therapy; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Neovascularization, Pathologic; prevention & control; Tongue Neoplasms; blood supply; genetics; prevention & control; Transfection; Tumor Cells, Cultured
- From: Chinese Journal of Stomatology 2004;39(4):273-276
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSLipofectamine-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).
RESULTSThe 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%.
CONCLUSIONShES 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.