Research On Effect Of Licl Inhibiting Glioma U251 Cell Proliferation And GSK-3β Expression

Introduction:Glioma is the most co mmol/lon primary cranial nerve epithelial neoplasms,which is the major threat to human health after stroke in nervous system disease;The high recurrence rate,high morbidity,high mortality make it difficult to cure;Surgical resection with radiotherapy and chemotherapy is the main means ,but its effect is not optimistic and it is i mmol/linent to look for effective ways to improve the prognosis and high quality life of new treatments. The pathogenesis of gliomas still not clear probe into the origin and development of gliomas molecular mechanism will contribute to better understand its incidence process provides a new way for clinical treatment.Glycogen synthase kinase-3(GSK-3)is a serine/threonine kinase,highly conserved and has been identified in every eukaryote.It is encoded by two isoforms in ma mmol/lal stermed GSK-3αand GSK-3β.It plays an important role in motility and cell fate,Now GSK-3 plays an important role in at least three signal transductory systems namely the Wnt/ wingles,NF-κB and GSK-3βwhich are closely related with tumor.Regulation activity of GSK-3 can influence survival and proliferation of tumor.GSK-3 deserves further study to provide valuable targets for potential anti-cancer therapeutic agents. Recent studies show that GSK - 3βmutation or down-expressing can promote breast tumors.LiCl (LiCl), a GSK - 3βinhibitor in many reports is a relatively single-minded inhibitors and need a relatively high doses (restrain constant Ki for mmol/l level) to inhibite GSK - 3βactivity its mechanism is competitive with Mg2 +. In mice test study,Li+ can increased GSK - 3βser9 phosphorylation thus inhibiting GSK - 3βactivity;The long-term use of Li+ didn't cause cancer risk which is widely used as GSK - 3βinhibitors. Many studies show that a lot of signaling transduction pathways abnormal activation or mechanism involving an GSK - 3βin tumor growth process;However, the results are different between domestic and international , this study aims to explore GSK - 3 inhibitors role in gliomas cell proliferation.PurposeTo investigate the influence of glioma U251 cell proliferation with the use of GSK - 3βinhibitor(LiCl),and GSK - 3βexpression.Method:U251 cells were cultivate in DMEM medium contain 10% heat-inactivated fetal calf serum in 37℃5% saturated humidity incubator CO2 nestin) to cultivate, continuous growth after inoculation logarithmic in 24 hours, using different growth reached logarithm LiCl 24h respectively U251 concentration of role 48h, The inhibitory effects of U251 cells proliferation were assayed with MTT test, Flow cytometry was used to investigate the distribution of cell cycle;I mmol/lunohistochemical testing was to detect GSK - 3βprotein expression. Using statistical software SPSS13.0 to analyse experimental data.Result:Different concentrations of LiCl reacting on U251 glioma, MTT test showed U251 cell proliferation is clearly influenced by LiCl; Flow cytometry showed U251 cells detection instrument cell cycle happened obviously change significantly reduce cell proliferation period; I mmol/lunohistochemical test showed GSK - 3βprotein expression significantly increasing, especially in the nucleus.Conclusion:LiCl ,GSK - 3βinhibitor, can significantly suppress glioma U251 cells proliferation, and up-regulating GSK-3βprotein expression.