Down-regulation of MHC class I antigens is not a general mechanism for the increased tumorigenicity caused by c-myc amplification.
Previous studies have shown that increased expression of oncogenes from the myc-family can down-regulate the level of MHC class I antigens in tumor cells. This has suggested a mechanism by which amplification/overexpression of myc-genes may contribute to the malignancy development of certain tumors. Earlier published data from the murine SEWA tumor, a polyomavirus-induced osteosarcoma, have correlated the degree of tumorigenicity of different sublines to their level of c-myc amplification. Here I present a quantitative and qualitative analysis of MHC class I antigens from five sublines of this tumor system. No differences could be found, between sublines with different degrees of tumorigenicity, regarding MHC class I antigen expression. Thus, in the SEWA tumor, the enhancement of the tumorigenicity caused by c-myc amplification is not mediated through down-regulation of MHC class I antigens.
Dahllöf
B
B
Ludwig Institute for Cancer Research, Stockholm, Sweden.
D000818:Animals; D003001:Cloning, Molecular; D005784:Gene Amplification; D005805:Genes, MHC Class I; D005809:Genes, Regulator; D015395:Histocompatibility Antigens Class I / Q000235:genetics; D051379:Mice; D005810:Multigene Family; D012516:Osteosarcoma / Q000235:genetics / Q000382:microbiology; D011120:Polyomavirus / Q000235:genetics; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016271:Proto-Oncogene Proteins c-myc; D011519:Proto-Oncogenes; D012513:Sarcoma, Experimental / Q000235:genetics / Q000382:microbiology
D015395:Histocompatibility Antigens Class I; D011518:Proto-Oncogene Proteins; D016271:Proto-Oncogene Proteins c-myc; D011505:Protein-Tyrosine Kinases