Objective: S100A6 (a.k.a., calcyclin) is over-expressed in several human tumors, including gastric carcinoma, human melanoma, pancreatic carcinoma, squamous cell carcinoma, malignant fibrous histiocytoma (MFH), and carcinomas of the thyroid, breast, and colon. However, little is known about the role S100A6 plays in gastric adenocarcinoma. In the present study, we intended to investigate the influence of S100A6 on the growth, proliferation, apoptosis, invasion and cell cycle of the gastric cancer cell MKN45. Methods: As an important member of S100 family, S100A6 cDNA was subcloned into a constitutive vector pcDNA3.1 followed by transfection in gastric cancer cell line MKN45 by using liposome. Then stable transfectants were selected and appraised. 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 S100A6 stable expression clones (MKN-S100A6) were detected and compared with their control groups respectively. Results: MKN-S100A6 grew faster than MKN45 and MKN-PC (MKN45 transfected with pcDNA3.1 vector). The cell counts of MKN-S100A6 in the fifth, sixth and seventh days were significantly more than those of control groups (P < 0.05). Cell cycle analysis showed that proportions of MKN-S100A6 in G0-G1 and G2-M were different significantly with those of its control groups respectively (P < 0.05). The apoptosis rate of MKN-S100A6 was significantly lower than those of control groups (P < 0.05). Results of colony-forming assay showed that the colon formation rate of MKN-S100A6 was higher than those of control groups (P < 0.05). Conclusion: S100A6 can promote the growth and proliferation of gastric cancer cells. It can help tumor cell maintain malignant phenotype. In gastric cancer, S100A6 could be thought as a tumor-enhancing gene in some distance, but its role could be complicated.
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