Effects of canstatin gene transfection on growth and apoptosis of lung cancer A549 cells and HUV-ECC cells.
- Author:
Weizhong LU
1
;
Guijun HUANG
;
Guisheng QIAN
;
Yuying LI
;
Shicang YU
;
Jin LI
Author Information
- Publication Type:Journal Article
- From: Chinese Journal of Lung Cancer 2005;8(2):95-98
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUNDAngiogenesis is essential for tumor's growth and metastasis. Canstatin, a newly found potent endogenous angiogenesis inhibitor, has drawn researcher's attention to its powerful biological activities on endothelial cells. The aim of this experiment is to explore the expression and effects of canstatin gene in lung cancer A549 cells and HUV-ECC cells.
METHODSExpression vector of pCMV- Script/Canstatin was transfected into A549 and ECC cells by electroporation, and the positive clone was screened by G418. Growth characteristics of the two cell lines were compared before and after transfection. Expression of canstatin protein in supernatant was examined by SDS-PAGE assay, and cell cycles of the two cell lines were analysed by flow cytometry.
RESULTSThe expression of canstatin gene was found in supernatant of the transfected A549 cells and ECC cells. The apoptotic rate in the transfected ECC cells (16.04%) was significantly increased compared with that of the naked plasmid control group (0.43%) and parental cell group (2.92%) (P < 0.01). The growth of the transfected ECC cells was significantly inhibited (P < 0.01). The apoptotic rate in the transfected A549 cells (0.19%) showed no marked difference from the naked plasmid control group (0.13%) and parental cell group (0.07%) (P > 0.05). No significant difference in cell growth was found among the transfected A549 cell, naked plasmid control and parental cell groups.
CONCLUSIONSThe results indicate that canstatin gene can express in lung cancer A549 cell line and HUV-ECC cell line, and it can specifically inhibit proliferation of endothelial cell and induce its apoptosis.