NR2B介导ERK信号通路对肝癌细胞增殖的影响

Effect of NR2B on proliferation of hepatocellular carcinoma cells through ERK signaling pathway

目的探讨N-甲基-D-天冬氨酸(NMDA)受体2B亚单位(NR2B)介导细胞外调节蛋白激酶(ERK)信号通路对肝癌细胞增殖的影响。方法检测8例肝癌组织及其癌旁组织中NR2B的表达,用NR2B激动剂NMDA、拮抗剂Ro25-6981和ERK通路抑制剂AZD8330处理肝癌细胞株SK-Hep1,分析NR2B和ERK信号通路对肝癌细胞增殖的影响。结果 NR2B在7例肝癌组织中表达上调(P<0.05)。NR2B拮抗剂Ro25-6981抑制肝癌细胞增殖(P<0.05),激动剂NMDA促进肝癌细胞增殖(P<0.05)。NR2B、磷酸化ERK和增殖细胞核抗原的表达随着NMDA浓度的增加而增加(P<0.05),随着Ro25-6981浓度的增加而降低(P<0.05)。ERK通路抑制剂AZD8330处理后,肝癌细胞增殖减弱(P<0.05),在此基础上用NMDA和Ro25-6981处理细胞,细胞增殖无明显变化(P>0.05)。结论 NR2B可通过ERK信号通路促进肝癌细胞的增殖。

Objective To investigate the effect of nmethyl-daspartic acid receptor 2 Bsubunit(NR2 B)on the proliferation of hepatocellular carcinoma(HCC)cells through extracellular regulated protein kinase(ERK)signaling pathway.Methods The expressions of NR2 Bin HCC tissues of 8 cases and HCC adjacent tissues were detected.The HCC cell line SK-Hep1 was treated with NR2 B agonist NMDA,NR2 B inhibitor Ro25-6981 and ERK signaling pathway inhibitor AZD8330,respectively.The cell proliferation of HCC cells was detected.Results The expression of NR2 Bwas higher in HCC tissues of 7 cases(P<0.05).NR2 Binhibitor Ro25-6981 inhibited the cell proliferation of HCC cells and agonist NMDA promoted the cell proliferation(P<0.05).The expressions of NR2 B,phosphorylation of ERK and proliferating cell nuclear antigen were increased with the increase of NMDA concentration(P<0.05),which were decreased with the increase of Ro25-6981 concentration(P<0.05).ERK signaling pathway inhibitor AZD8330 inhibited the cell proliferation(P<0.05),which was not affected by NMDA and Ro25-6981(P>0.05).Conclusion NR2 Bcan promote the proliferation of HCC cells through ERK signaling pathway.