Role Of ERK1/2 Signaling Pathway In Gastrin-induced Cell Proliferation And Apoptosis Of Large Intestinal Cancer And Regulation Mechanisms Study

Objective:In this study,Applying RNA interference technique to silence the ERK1/2 g enes by culturing them on vitro cells..Toanalyze the m RNAs total of ERK gene, expres sion of downstream target protein, and its phosphorylation level, in order to explore wh ether gastrin can regulate the proliferation of colon cancer cells by ERK1 / 2 signaling molecule signal transduction, and to further clarify the molecular mechanisms regulati ng the development of colorectal cancer, providing a theoretical basis for individualize d treatment of hormone-dependent part of colorectal cancer.Methods :RTQ-PCR detected the expression of gastrin receptor(CCK-2R) m RNA in CACO2 cells. MTT assay investigated the apoptosis change of CACO2 cells and determined the optimal concertration of pentagastrin to intervene the cell apoptosis. Cell experiment is divided into four groups. The expression of ERK1/2 protein levels were detected by Western blot.Results: q RT-PCR test results showed that CCK-2R m RNA was expressed of in the CACO2 cells.Pentagastrin inhibited CACO2 cells apoptosis in a dose dependent manner(6.25-200mg/L), and optimal dose is 25.00mg/L(P<0.05).Use Western-blot to detect differences in four groups of ERK protein expression levels(P<0.01).Conclusion : Gastrin can promote the human colon cancer cell line ERK1/2 enhance their proliferation, the expression of ERK1/2 was promoted. ERK1/2-sh RNA could effectively inhibit the expression of ERK1/2 and inhibite the cells proliferation of colorectal cancer. Gastrin perhaps regulates the cells proliferation of colorectal cancer by signal transduction pathway of ERK1/2 ways.