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作 者:徐智[1] 阳书华[1] 王恺[1] 黄明文[1] 邹书兵[1]
机构地区:[1]南昌大学第二附属医院肝胆外科,江西南昌330006
出 处:《中国病理生理杂志》2011年第1期108-112,共5页Chinese Journal of Pathophysiology
基 金:江西省教育厅基金资助项目(No.GJJ09092)
摘 要:目的:研究葡萄糖调节蛋白78(GRP78)在不同转移潜能肝癌细胞株内的表达及其对肝癌细胞生物学行为的影响。方法:应用GRP78反义寡核苷酸(GRP78 ASODN)转染肝癌细胞株HepG2和MHCC97-H。逆转录聚合酶链式反应(RT-PCR)技术检测肝癌细胞内GRP78 mRNA的表达,Transwell小室实验和细胞黏附实验分别检测2种肝癌细胞的侵袭、迁移及黏附能力。结果:2种细胞内均有GRP78的表达,MHCC97-H细胞表达较HepG2高(P<0.05)。GRP78 ASODN可以有效地抑制2种肝癌细胞株内GRP78的表达。GRP78 ASODN转染的高侵袭潜能的MHCC97-H肝癌细胞的侵袭、迁移和黏附能力较对照组有明显的下降(P<0.05),而低侵袭潜能的HepG2肝癌细胞侵袭、迁移及黏附能力下降不明显(P>0.05)。结论:抑制肝癌细胞内GRP78的表达可以削弱其侵袭、迁移及黏附能力,GRP78可能成为肝癌治疗上有效的分子靶点。AIM:To explore the effect of glucose-regulated protein 78(GRP78)expression on the biological behaviors of hepatocellular carcinoma cells with different metastatic potentials.METHODS:The GRP78 antisense oligonucleotide(GRP78 ASODN) was transfected into hepatocellular carcinoma cell lines,HepG2 and MHCC97-H.The mRNA expression of GRP78 in the two cell lines was assessed by RT-PCR.Transwell chamber assay was used to detect the cell invasion and migration.Cell adhesion assay was employed to investigate the cell adhesion.RESULTS:The positive GRP78 expression was observed in both HepG2 and MHCC97-H cells.The expression level of GRP78 in MHCC97-H cells was higher than that in HepG2 cells.GRP78 expression was effectively depressed by the transfection of GRP78 ASODN in both cell lines.The invasive,migratory and adhesive potentials of MHCC97-H cells after GRP78 ASODN transfection were more significantly depressed than those of HepG2 cells(P〈0.05).GRP78 ASODN transfection did not affect the biological behaviors of HepG2 cells.CONCLUSION:Inhibition of GRP78 expression in hepatocellular carcinoma cell lines depresses the cell invasion,migration and adhesion,indicating that GRP78 is a prospective molecular therapy target in hepatocellular carcinoma.
关 键 词:葡萄糖调节蛋白78 HEPG2细胞 MHCC97-H细胞 侵袭 转移
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