中文摘要：

客观 S100A6 (又名， calcyclin ) 在几个人的肿瘤，包括的胃的癌，人的黑瘤，胰腺的癌，有鳞的房间癌，恶意的含纤维的 histiocytoma (MFH ) ，和甲状腺，胸，和冒号的癌是过去表示的。然而，很少在胃的腺癌对角色 S100A6 戏被知道。在现在的学习，我们打算在生长，增长， apoptosis，侵略和胃的癌症细胞 MKN45 的细胞周期上调查 S100A6 的影响。方法作为 S100 家庭，的一个重要成员， S100A6 cDNA 是克隆进使用 transfection 在胃的癌症房间线 MKN45 跟随的组成的向量 pcDNA3.1 的潜水艇脂肪一些。然后稳定的 transfectants 被选择并且估价。这些克隆的 apoptosis 和房间周期被使用流动 cytometric 试金分析。生长和增长被房间生长曲线和形成殖民地的试金分别地分析。S100A6 稳定的表达式克隆(MKN-S100A6 ) 被检测并且分别地与他们的控制相比组织。结果 MKN-S100A6 变得比 MKN45 和 MKNPC (有 pcDNA3.1 向量的 MKN45 transfected ) 快。在第五，第六和第七天内的 MKN-S100A6 的房间计数是显著地多于那些控制组(P 【 0.05 ) 。房间周期分析证明在 G0-G1 和 G2-M 的 MKN-S100A6 的比例分别地与它的控制组的那些显著地是不同的(P 【 0.05 ) 。MKN-S100A6 的 apoptosis 率是比控制组的那些显著地低的(P 【 0.05 ) 。形成殖民地的试金的结果证明 MKN-S100A6 的冒号形成率比控制组的那些高(P 【 0.05 ) 。结论 S100A6 能支持胃的癌症房间的生长和增长。它能帮助肿瘤房间维持恶意的显型。在胃的癌症， S100A6 能在某距离作为提高肿瘤的基因被认为，但是它的角色能是复杂的。

英文摘要：

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 cDNAwas 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-SI00A6 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.