Kamo Sting By P38 And P44/42MAPK Brain Signal Transduction Pathway In Tumor Cell Proliferation Star

Objective: Mitogen-activated protein kinase (MAPK) cascade is a eukaryotic cell-mediated extracellular signal response to an important intracellular signal transduction systems, mediate the body's cell growth, differentiation, division, death and the function of cell synchronization And other processes。Discovered in recent years MAPK in cell invasion and metastasis of malignant transformation and tumor plays an important role. . Have identified four human MAPK pathway, that is, extracellular signal-regulated kinase (ERK) pathway,c-Jun N-terminal kinase (JNK) / stress-activated protein kinase (SAPK) pathway, big mitogen-activated protein kinase (BMK ) / ERK5 pathway and the p38MAPK pathway. A variety of human cancer cells in the prevalence of persistent activation of MAPK, suggesting that the pathological deterioration of MAPK in the cell plays an important role in the process. Growth in tumor cells, different signaling pathway and inhibition of different, and different types of tumor cells MAPK signal transduction in different ways, appropriate regulation of different MAPK pathway activity in cancer prevention and treatment may have important clinical significance。MAPK pathway is mediated by EGFR signaling pathway of cells, MAPK may be involved in astrocytoma development and progression. Therefore, MAPK in astrocytoma clarify the signal transduction mechanisms, contribute to MAPK inhibitors in cancer prevention and treatment in clinical application.Methods: First,put U251 malignant glioma cells in cell culture, application kamo Sting observed inhibition of cell proliferation. Detected by immunohistochemical staining in human astrocytoma ERK1 / 2, p38MAPK, and phosphorylation of ERK1 / 2, the expression of phosphorylated p38MAPK.Western blotting detection of human astrocytomas and tumor tissue of ERK1 / 2, p38MAPK and phosphorylated ERK1 / 2, phosphorylated p38MAPK protein expression. compared with before treatment, but the p38MAPK and phosphorylated p38MAPK in the totals and ERK1/2MAPK.With the increase of drug concentration, kamo Sting on the role of U251 cells with deadly accuracy. Meanwhile, with the prolonged-treatment, the inhibition rate also rising trend. Drug concentration effect 250,500,1000 micrograms per milliliter for 24 hours, on U251 cell proliferation inhibition rates were 13.25%, 20.32% and 27.41%, we can see, within a certain range, the longer the drug can lead to more cell death.Results: Kamo Sting glioma cells the expression of phosphorylated p38MAPK more than before treatment, and phosphorylation of ERK1/2 protein expression decreasedConclusion:1.Kamo Sting inhibiting the proliferation of U251 cancer cells may be related to mitogen-activated protein kinase (MAPK) signal transduction pathway activation.2.Kamo Sting p38mapk by phosphorylation mediated activation of tumor cell cycle arrest and apoptosis signal transduction lead to malignant glioma cells proliferation.3.Kamo Sting can inhibit the expression of protein phosphorylation P44/42mapk, there may be inhibition of tumor cell proliferation.