The aim of this study was to investigate the influence of calcyclin on the growth, proliferation, apoptosis, invasion and cell cycle of gastric cancer cell lines in order to elucidate the role that calcyclin plays in gastric adenocarcinoma. Calcyclin cDNA was subcloned into a constitutive vector pcDNA3.1 followed by liposome-mediated transfection in the MKN45 gastric cancer cell line. Stable transfectants were selected and appraised. Specific inhibition of calcyclin was achieved using a vector-based siRNA system by transfection into the SGC7901 gastric cancer cell line. The apoptosis and cell cycle of these clones were analyzed by flow cytometry. Growth and proliferation were analyzed by cell growth curves and a colony-formation assay, respectively. The invasion of these clones was analyzed by a cell migration assay. MKN-calcyclin grew faster compared to MKN45 and MKN-PC (MKN45 transfected with pcDNA3.1 vector). SGC-SR1,2 grew slower compared to SGC7901 and SGC-SS1,2 (SGC7901 transfected with scrambled control duplexes). Cell cycle analysis showed that proportions of MKN-calcyclin and SGC-SR1,2 cells in G0/G1 and G2/M were significantly different compared to those of their control groups, respectively (P<0.05). The apoptosis rate of MKN-calcyclin was significantly lower compared to those of control groups (P<0.05). Results of colony-formation assay showed that the colony formation rate of MKN-calcyclin was higher compared to those of control groups, otherwise the rates of SGC-SR1,2 were lower compared to those of their control groups (P<0.05). The results of the cell migration assay showed that the migration rate of MKN-calcyclin was significant lower compared to those of its control groups, conversely, the migration rates of SGC-SR1,2 were significantly higher than those of their control groups (P<0.05). In conclusion, calcyclin can promote the growth and proliferation of gastric cancer cells and knockdown of calcyclin can restrain the growth and proliferation of gastric cancer cells. It can help tumor cells maintain the malignant phenotype. However, it can depress the ability of invasion of gastric cancer cells, thus restraining the metastasis of gastric cancer.

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