The upregulation or mutation of C-MYC has been observed in gastric, colon, 
breast, and lung tumors and in Burkitt's lymphoma. However, little is known 
about the role C-MYC plays in gastric adenocarcinoma. In the present study, we 
intended to investigate the influence of C-MYC on the growth, proliferation, 
apoptosis, invasion, and cell cycle of the gastric cancer cell line SGC7901 and 
the gastric cell line HFE145. C-MYC cDNA was subcloned into a constitutive 
vector PCDNA3.1 followed by transfection in normal gastric cell line HFE145 by 
using liposome. Then stable transfectants were selected and appraised. Specific 
inhibition of C-MYC was achieved using a vector-based siRNA system which was 
transfected in gastric cancer cell line SGC7901. The apoptosis and cell cycles 
of these clones were analyzed by using flow cytometric assay. The growth and 
proliferation were analyzed by cell growth curves and colony-forming assay, 
respectively. The invasion of these clones was analyzed by using cell migration 
assay. The C-MYC stable expression clones (HFE-Myc) and C-MYC RNAi cells 
(SGC-MR) were detected and compared with their control groups, respectively. 
HFE-Myc grew faster than HFE145 and HFE-PC (HFE145 transfected with PCDNA3.1 
vector). SGC-MR1, 2 grew slower than SGC7901 and SGC-MS1, 2 (SGC7901 transfected 
with scrambled control duplexes). The cell counts of HFE-Myc in the third, 
fourth, fifth, sixth, and seventh days were significantly more than those of 
control groups (P < 0.05). Those of SGC-MR1, 2 in the fourth, fifth, sixth, and 
seventh days were significantly fewer than those of control groups (P < 0.05). 
Cell cycle analysis showed that proportions of HFE-Myc and SGC-MR cells in G0-G1 
and G2-M were different significantly with their control groups, respectively (P 
< 0.05). The apoptosis rate of HFE-Myc was significantly higher than those of 
control groups (P < 0.05). Results of colony-forming assay showed that the 
colony formation rate of HFE-Myc was higher than those of control groups; 
otherwise, the rate of SGC-MR was lower than those of their control groups (P < 
0.05). The results of cell migration assay showed that there were no significant 
differences between experimental groups and control groups (P > 0.05). In 
conclusion, C-MYC can promote the growth and proliferation of normal gastric 
cells, and knockdown of C-MYC can restrain the growth and proliferation of 
gastric cancer cells. It can induce cell apoptosis and help tumor cell maintain 
malignant phenotype. But it can have not a detectable influence on the ability 
of invasion of gastric cancer cells.