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EXPRESSION OF FLIP IN HUMAN COLON CARCINOMAS: A NEW MECHANISM OF IMMUNE EVASION 被引量:1

EXPRESSION OF FLIP IN HUMAN COLON CARCINOMAS: A NEW MECHANISM OF IMMUNE EVASION
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摘要 Objective: It has been proposed that Fas ligand (FasL) may play an important role in immune escape of tumors and FLIP is an important mediator of Fas/FasL pathway. In this study, the expression of FLIP was determined in human colon carcinoma cell lines and tissue to investigate the new mechanism of immune evasion of human colon carcinomas. Methods: RT-PCR and immunohistochemistry (IHC) were performed to investigate the expression of FLIP in human colon carcinoma cell lines SW480, LS174 and twenty human primary colon carcinoma specimens. Results: It was shown that SW480 cells, LS174 cells and primary colon carcinoma specimen constitutively expressed FLIP at the mRNA and protein level. The expression of FLIP was not found in the epithelial cells of normal colon mucosa. Conclusion: FLIP was expressed in human primary colon carcinoma specimens but not in the normal counterpart. It suggested that the expression of FLIP may occur during the malignant transformation from normal colon epithelial cells to colon carcinoma cells. Tumor cells might obtain the ability to resist the Fas-mediated apoptosis by expressing FLIP. The expression of FLIP might contribute to the formation of colon carcinomas. Objective: It has been proposed that Fas ligand (FasL) may play an important role in immune escape of tumors and FLIP is an important mediator of Fas/FasL pathway. In this study, the expression of FLIP was determined in human colon carcinoma cell lines and tissue to investigate the new mechanism of immune evasion of human colon carcinomas. Methods: RT-PCR and immunohistochemistry (IHC) were performed to investigate the expression of FLIP in human colon carcinoma cell lines SW480, LS174 and twenty human primary colon carcinoma specimens. Results: It was shown that SW480 cells, LS174 cells and primary colon carcinoma specimen constitutively expressed FLIP at the mRNA and protein level. The expression of FLIP was not found in the epithelial cells of normal colon mucosa. Conclusion: FLIP was expressed in human primary colon carcinoma specimens but not in the normal counterpart. It suggested that the expression of FLIP may occur during the malignant transformation from normal colon epithelial cells to colon carcinoma cells. Tumor cells might obtain the ability to resist the Fas-mediated apoptosis by expressing FLIP. The expression of FLIP might contribute to the formation of colon carcinomas.
出处 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2005年第3期193-198,共6页 中国癌症研究(英文版)
关键词 Colon carcinoma FAS/FASL FLIP Immune evasion Colon carcinoma Fas/FasL FLIP Immune evasion
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  • 1YoneharaS,IshiiA,YoneharaM.A cell-killing monoclonal antibody(anti-Fas) to a cell surface antigen co-downregulated with the receptor of tumor necrosis factor[].The Journal of Experimental Medicine.1989
  • 2StrandS,HofmannWJ,HugH,et al.Lymphocyte apoptosis induced byCD95(APO-1/Fas) ligand-expressing tumor cells:A mechanism of immune evasion[].NatMed.1996
  • 3NagataS.Fas ligand and immune evasion[].NatMed.1996
  • 4SaasP,WalkerPR,HahneM,et al.Fas ligand expression by astrocytoma in vivo: maintaining immune privilege in the brain[].The Journal of Clinical Investigation.1997
  • 5HugH.Fas-mediated apoptosis in tumor formation and defense[].Journal of Biochemistry.1997
  • 6HahneM,RimoldiD,Schr鰐erM,et al.Melanoma cell expression ofFas(APO-1/CD95) ligand:Implications for tumor immune escape[].Science.1997
  • 7WalkerPR,SaasP,DietrichPY.Role ofFas ligand(CD95L) in immune escape: the tumor cell strikes back[].J Immunol.1997
  • 8NagataS.Apoptosis by death factor[].Cell.1997
  • 9NichansGA,BrunnerT,FrizelleSP,et al.Human lung carcinomas expressFas ligand[].Cancer Research.1997
  • 10BuechnerSA,WernliM,HarrT,et al.Regression of basal cell carcinoma by intralesional interferon-alpha treatment is mediated byCD95(APO-1/Fas)-CD95 ligand-induced suicide[].The Journal of Clinical Investigation.1997

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