| Gastric cancer occurs with a high incidence in Asia and is one of the leading causes of cancer death in the world. Although the incidence and mortality of gastric carcinoma are decreasing in many countries, gastric cancer still represents the second most frequent malignancy in the world. The major site of gastrin synthesis and secretion is the gastrin-containing cell (G cell) in the antropyloric mucosa. Gastrin is now firmly established as the physiological regulator of gastric acid secretion and an important regulator of gastric mucosal cell proliferation. The presence of a potential gastrin autocrine/paracrine pathway has been reported to exist in gastric cancer cell lines. Gastrin has been shown to be a growth factor for gastric tumours in established BGC-823 cell lines. Furthermore, malignant cells were shown to have heightened sensitivity to the proliferative effects of gastrin when compared with corresponding normal gastric epithelial cells. The gastrin expression rate in gastric carcinoma patients was 47.7% (133/279). Gastrin also exert anti-apoptotic effects, amd may play an important role in invasion and metastasis. Therefore, gastrin gene may provide a potential target for genetic therapy of gastric cancer.RNA interference (RNAi), as commonly defined, is a phenomenon leading to post-transcriptional gene silencing (PTGS) after endogenous production or artificial introduction into a cell of small interfering double strand RNA with complementary sequences to the targeted gene. RNAi has been successfully used to suppress gene expression in a variety of organisms including zebrafish, Caenorhabditis elegans, Drosophila, planaria, mice, and mammalian cells. Possible repercussions of RNAi in mammals arc its use in the fight against certain diseases, such as cancer. In mammalian cells, RNAi was first employed as a tool to induce the silencing of the targeted gene. |
