Down-regulation of MHC class I antigens is not a general mechanism for the increased tumorigenicity caused by c-myc amplification.

Abstract

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.

• Authors: B Dahllöf
• Journal: Oncogene (Oncogene) Vol. 5 Issue 3 Pg. 433-5 (Mar 1990) ISSN: 0950-9232 [Print] England
• PMID: 2156210 (Publication Type: Journal Article)

Chemical References

• Histocompatibility Antigens Class I
• Proto-Oncogene Proteins
• Proto-Oncogene Proteins c-myc
• Protein-Tyrosine Kinases

Topics

• Animals
• Cloning, Molecular
• Gene Amplification
• Genes, MHC Class I
• Genes, Regulator
• Histocompatibility Antigens Class I (genetics)
• Mice
• Multigene Family
• Osteosarcoma (genetics, microbiology)
• Polyomavirus (genetics)
• Protein-Tyrosine Kinases (genetics)
• Proto-Oncogene Proteins (genetics)
• Proto-Oncogene Proteins c-myc
• Proto-Oncogenes
• Sarcoma, Experimental (genetics, microbiology)