Yamit-Hezi A, Plaksin D, Eisenbach L
Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Oncogene. 1994 Apr;9(4):1065-79.
Reduced co-expression of the c-fos and c-jun protooncogenes has been correlated with the down regulation of H-2K class I major histocompatibility antigens in high-metastatic cell lines from the Lewis lung carcinoma, B16 melanoma and the K1735 melanoma. Transfection of c-jun and c-fos genes into the high metastatic clones D122 (3LL) and F10.9 (B16 melanoma) resulted in activation of H-2 class I gene expression. D122 transfectants expressing high levels of c-jun and c-fos and F10.9 transfectants expressing high levels of c-fos exhibited markedly reduced tumorigenicity and were of low metastatic potential. In contrast, transfection of junB into the low metastatic, high H-2Kb, Db expressor clone A9 (3LL), reduced MHC class I gene expression, and converted the parental low, into high-metastatic cells. The data demonstrate the involvement of genes from the fos and jun family in regulation of MHC class I expression and consequently in regulation of immunogenicity and metastatic competence of tumor cells.
在源自Lewis肺癌、B16黑色素瘤和K1735黑色素瘤的高转移细胞系中，原癌基因c-fos和c-jun的共表达降低与I类主要组织相容性抗原H-2K的下调相关。将c-jun和c-fos基因转染至高转移克隆D122（3LL）和F10.9（B16黑色素瘤）中，导致I类H-2基因表达激活。表达高水平c-jun和c-fos的D122转染子以及表达高水平c-fos的F10.9转染子显示出明显降低的致瘤性且转移潜力较低。相反，将junB转染至低转移、高表达H-2Kb和Db的克隆A9（3LL）中，降低了MHC I类基因表达，并将亲代低转移细胞转变为高转移细胞。数据表明fos和jun家族基因参与MHC I类表达的调控，进而参与肿瘤细胞免疫原性和转移能力的调控。
