解剖学报
解剖學報
해부학보
ACTA ANATOMICA SINICA
2009年
6期
928-932
,共5页
苏荣健%李贞%程留芳%李宏丹%魏嘉%包翠芬
囌榮健%李貞%程留芳%李宏丹%魏嘉%包翠芬
소영건%리정%정류방%리굉단%위가%포취분
肝细胞癌%Grp78%细胞外信号调节激酶1/2%小RNA干扰%SMMC-7721%免疫组织化学%免疫印迹法%人
肝細胞癌%Grp78%細胞外信號調節激酶1/2%小RNA榦擾%SMMC-7721%免疫組織化學%免疫印跡法%人
간세포암%Grp78%세포외신호조절격매1/2%소RNA간우%SMMC-7721%면역조직화학%면역인적법%인
Hepatocellular carcinoma%Grp78%ERK1/2%siRNA%SMMC-7721%Immunohistochemistry%Western blotting%Human
目的 通过检测葡萄糖调节蛋白78(Grp78)、细胞外信号调节激酶(ERK1/2)、磷酸化ERK1/2在肝细胞癌手术切除组织中的表达,并在SMMC-7721细胞中干预Grp78的表达,探讨Grp78对ERK1/2激酶的调控作用. 方法 应用免疫组织化学方法(IHC)和免疫印迹法检测47例肝细胞癌手术切除组织样本中Grp78,ERK1/2的表达和ERK1/2磷酸化水平;在高表达Grp78的肝细胞癌细胞系SMMC-7721中,通过用小RNA干扰Grp78的表达来探讨Grp78表达水平,改变对ERK1/2活性及表达的影响. 结果 在肝细胞癌组织样本中,Grp78的表达情况与ERK1/2和磷酸化ERK1/2的表达明显呈正相关.在SMMC-7721细胞中Grp78高表达促进ERK1/2的磷酸化,应用RNA干扰特异性下调Grp78高表达细胞中Grp78水平可以抑制ERK1/2的磷酸化. 结论 Grp78参与调解ERK1/2信号通路,并且在肝细胞癌临床治疗方面可能成为潜在的治疗靶点.
目的 通過檢測葡萄糖調節蛋白78(Grp78)、細胞外信號調節激酶(ERK1/2)、燐痠化ERK1/2在肝細胞癌手術切除組織中的錶達,併在SMMC-7721細胞中榦預Grp78的錶達,探討Grp78對ERK1/2激酶的調控作用. 方法 應用免疫組織化學方法(IHC)和免疫印跡法檢測47例肝細胞癌手術切除組織樣本中Grp78,ERK1/2的錶達和ERK1/2燐痠化水平;在高錶達Grp78的肝細胞癌細胞繫SMMC-7721中,通過用小RNA榦擾Grp78的錶達來探討Grp78錶達水平,改變對ERK1/2活性及錶達的影響. 結果 在肝細胞癌組織樣本中,Grp78的錶達情況與ERK1/2和燐痠化ERK1/2的錶達明顯呈正相關.在SMMC-7721細胞中Grp78高錶達促進ERK1/2的燐痠化,應用RNA榦擾特異性下調Grp78高錶達細胞中Grp78水平可以抑製ERK1/2的燐痠化. 結論 Grp78參與調解ERK1/2信號通路,併且在肝細胞癌臨床治療方麵可能成為潛在的治療靶點.
목적 통과검측포도당조절단백78(Grp78)、세포외신호조절격매(ERK1/2)、린산화ERK1/2재간세포암수술절제조직중적표체,병재SMMC-7721세포중간예Grp78적표체,탐토Grp78대ERK1/2격매적조공작용. 방법 응용면역조직화학방법(IHC)화면역인적법검측47례간세포암수술절제조직양본중Grp78,ERK1/2적표체화ERK1/2린산화수평;재고표체Grp78적간세포암세포계SMMC-7721중,통과용소RNA간우Grp78적표체래탐토Grp78표체수평,개변대ERK1/2활성급표체적영향. 결과 재간세포암조직양본중,Grp78적표체정황여ERK1/2화린산화ERK1/2적표체명현정정상관.재SMMC-7721세포중Grp78고표체촉진ERK1/2적린산화,응용RNA간우특이성하조Grp78고표체세포중Grp78수평가이억제ERK1/2적린산화. 결론 Grp78삼여조해ERK1/2신호통로,병차재간세포암림상치료방면가능성위잠재적치료파점.
Objective We examined the Grp78, ERK1/2 and phospho-ERK1/2 expressions in hepatocellular carcinoma(HCC) tissue samples in vitro, we interfered the expression of Grp78 in SMMC-7721 cells to explore whether Grp78 is involved in ERK1/2 signal pathway. Methods The Grp78, ERK1/2 and phospho-ERK1/2 expressions were detected by immunohistochemistry and confirmed by Western blotting in 47 HCC tissue samples. The Grp78 expression in SMMC-7721 cells was interfered by plasmid transfection and siRNA, ERK1/2 phosphorylation and expression were determined by Western blotting. Results The Grp78 expression was significantly correlated with ERK1/2 and phospho-ERK1/2 in HCC tissue samples. Overexpression of Grp78 promoted ERK1/2 phosphorylation in SMMC-7721 cells and the increased ERK1/2 phosphorylation was inhibited by Grp78 knockdown. Conclusion Grp78 is involved in the regulation of ERK1/2 signal pathway and might be a potential target for the comprehensive therapy of HCC.
