论文部分内容阅读
应用基因芯片技术筛选胃腺癌转移相关基因的过程中 ,发现CDK抑制因子 (CKI)P18INK4C在人类胃腺癌转移细胞株RF 4 8中的表达 ,较其原发灶细胞株RF 1明显下调。这提示 ,P18INK4C表达差异与胃腺癌细胞的侵袭转移 ,可能有一定程度的相关性。为此 ,通过反义RNA技术抑制在RF 1中的表达 ,研究其对胃腺癌原发灶细胞体外运动、侵袭转移能力以及生长特性的影响 ,进一步明确P18INK4C与人类胃腺癌侵袭转移之间的关系。结果发现 ,抑制P18INK4C的表达 ,可以使胃腺癌原发灶细胞的体外侵袭能力明显增加 ,抑制前RF 1细胞的体外侵袭能力仅为抑制后的 4 4 %。然而 ,RF 1的细胞周期和生长增殖能力 ,并未因为P18INK4C表达的改变而受到影响。上述结果提示 ,P18INK4C参与人类胃腺癌转移过程 ;在此过程中 ,其主要的作用可能并不是调节细胞周期 ,而是与胃腺癌原发灶细胞侵袭转移能力的调节密切相关。
In the course of screening genes related to metastasis of gastric adenocarcinoma using gene chip technology, it was found that the expression of CDK inhibitor (CKI) P18INK4C in human gastric adenocarcinoma metastatic cell line RF 4 8 was significantly downregulated compared with its primary tumor cell line RF 1. This suggests that there may be a certain degree of correlation between P18INK4C expression and the invasion and metastasis of gastric adenocarcinoma cells. To this end, antisense RNA technology was used to suppress the expression in RF 1 and its effects on the in vitro movement, invasion, metastasis and growth characteristics of gastric adenocarcinoma primary tumor cells were studied to further clarify the relationship between P18INK4C and invasion and metastasis of human gastric adenocarcinoma. . The results showed that inhibiting the expression of P18INK4C could increase the invasive ability of gastric adenocarcinoma primary tumor cells in vitro, and the in vitro invasive ability of the inhibited RF 1 cells was only 44% after inhibition. However, the cell cycle and growth proliferative capacity of RF 1 were not affected by changes in P18INK4C expression. The above results suggest that P18INK4C is involved in the metastasis of human gastric adenocarcinoma; in this process, its main role may not be to regulate the cell cycle, but is closely related to the regulation of the invasion and metastasis capacity of gastric adenocarcinoma primary tumor cells.