期刊文献+

热休克蛋白70和糖调节蛋白94在人胃癌细胞BGC-823中的表达

Expression and significance of heat shock protein 70 and glucose - regulated protein 94 in human gastric carcinoma BGC-823 cell line
下载PDF
导出
摘要 目的 :探讨热休克蛋白 70 ( HSP70 )和糖调节蛋白 94( grp94)在人胃癌细胞BGC- 82 3中的表达及其意义。方法 :利用 En Vision免疫细胞化学、双抗体标记免疫荧光和流式细胞仪方法检测和分析人胃癌细胞 BGC- 82 3中 HSP70和grp94的表达及其与细胞周期的关系。结果 :胃癌细胞存在 HSP70和 grp94的高表达 ,免疫细胞化学显示 HSP70和 grp94主要定位于胞浆 ;免疫荧光法和流式细胞仪检测显示 HSP70的表达阳性率为 84.9% ,grp94为 79.7% ,与阴性对照组存在明显的差异 ;在整个细胞周期均存在 HSP70和 grp94的持续表达。结论 :胃癌细胞存在 HSP70和 grp94的高表达 ,在整个细胞周期 HSP70和 grp94均持续表达 ,其表达与细胞周期无明显关系。 HSP70和 grp94在人胃癌细胞中的表达特点为瘤苗的研究奠定了基础。 Objective: To study expression and si gnificance of HSP70 and grp94 in human gastric carcinoma BGC-823. Methods: Gastric carcinoma BGC-823 cell slide s were collected. HSP70 and grp94 expression was detected by immunochemistry, do uble-labelled antibodies immunoinfluresent. The relationship between HSP70,grp9 4 and cell growth cycle was analized by FACS. Results: Compared with controll gr oup, gastric cancer BGC-823 cells expressed high level of HSP70 and grp94,which were localized in cellular cytoplasm. DNA content analysis revealed that HSP70 and grp94 were expressed continuously throughout the whole cell cycle. Conclusio n: Human gastric carcinoma BGC-823 cells had high level expression of HSP70 and grp94 through the whole cell cycle. FACS analysis showed that there was no rel ationship between expression of HSP70, grp94 and cell cycle. The study on expres sion of HSP70 and grp94 in human gastric carcinoma BGC-823 will lay a basis for further research on anti-tumor immunotherapy.
出处 《陕西医学杂志》 CAS 北大核心 2005年第3期334-336,共3页 Shaanxi Medical Journal
基金 北京市青年科技骨干基金资助 (0 2 1 2 0 0 3 1 )
关键词 GRP94 HSP70 高表达 人胃癌细胞 糖调节蛋白94 细胞周期 热休克蛋白70 免疫细胞化学 免疫荧光法 流式细胞仪 Heat shock protein 70/immunol ogy @Glucose-regulated protein 94 Stomach neoplasins/immunology
  • 相关文献

参考文献2

二级参考文献58

  • 1Seliger B, Ritz U, Abele R, Bock M, Tampe R, Sutter G, Drexler I,Huber C, Ferrone S. Immune escape of melanoma: first evidence of structural alterations in two distinct components of the MHC class I antigen processing pathway. Cancer Res 2001; 61:8647-8650.
  • 2Ritz U, M0mburg F, Pilch H, Huber C, Maeurer MJ, Seliger B.Deficient expression of components of the MHC class I antigen processing machinery in human cervical carcinoma. Int J Oncol 2001; 19:1211-1220.
  • 3Dovhey SE, Ghosh NS, Wright KL. Loss of interferon-gamma inducibility of TAP1 and LMP2 in a renal cell carcinoma cell line.Cancer Res 2000; 60:5789-5796.
  • 4Dressel R, Lubbers M, Waiter L, Herr W, Gunther E. Enhanced susceptibility to cytotoxic T lymphocytes without increase of MHC class. I antigen expression after conditional overexpression of heat shock protein 70 in target cells. Eur J Immunol 1999; 29:3925-3935.
  • 5Chen D, Androlewicz MJ. Heat shock protein 70 moderately enhances peptide binding and transport by the.transporter associated with antigen processing. Immunol Lett 2001; 75:143-148.
  • 6Kurokohchi K, Carrington IV[, Mann DL, Simonis TB, Alexander-Miller MA, Feinstone SM, Akatsuka T, Berzofsky JA. Expression of HLA class I molecules and the transporter associated with antigen processing in hepatocellular carcinoma. Hepatology 1996;23:1181-1188.
  • 7Alimonti J, Zhang QJ, Gabathuler R, Reid G, Chen SS, Jefferies WA. TAP expression provides a general method for improving the recognition of malignant cells in vivo. Nat Biotechnol 2000; 18:515-520.
  • 8Seliger B, Ritz U, Abele R, Bock M, Tampe R, Sutter G, Drexler LHuber C, Ferrone S.Immune escape of melanoma: first evidence of structural alterations in two distinct components of the MHC class I antigen processing pathway. Cancer Res 2001; 61: 8647-8650.
  • 9Seliger B, Bock M, Ritz U, Huber C. High frequency of a nonfunctional TAP1/LMP2 promoter polymorphism in human tumors. Int J Oncol 2002; 20:. 349-353.
  • 10Cromme FV, Airey J, Heemels MT, Ploegh HL, Keating PJ, Stern PL, Meijer CJ, Walboomers JM. Loss of transporter protein, encoded by the TAP-1 gene, is highly correlated with loss of HLA expression in cervical carcinomas. J Exp Med 1994; 179:335-340.

共引文献31

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部