Hassan Y, Priel E, Segal S, Huleihel M, Aboud M
Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel.
Carcinogenesis. 1990 Dec;11(12):2097-102. doi: 10.1093/carcin/11.12.2097.
We demonstrate in this study that infection with Moloney murine leukemia virus (M-MLV) and exposure to 3-methylcholanthrene (3-MC) can cooperate to transform NIH/3T3 mouse fibroblasts. M-MLV seems to stimulate the expression of c-myc and of a certain major histocompatibility complex (MHC) class I gene. Yet M-MLV infection by itself is insufficient to transform these cells. However, exposure of the infected cells to 3-MC resulted in a rapid cell transformation with concomitant enhancement of c-Ha-ras and H-2K class I MHC gene expression in the transformed cells. No such transformation was observed when uninfected NIH/3T3 cells were similarly treated with this carcinogen. Clones of cells transformed by this combined effect of M-MLV and 3-MC were found to be highly tumorigenic in fully immunocompetent allogeneic BALB/c mice. We provide evidence to suggest that the enhanced expression of the H-2K gene in these transformed cells plays an important role in overcoming the BALB/c allogeneic barrier and allowing tumor growth in these mice.
我们在本研究中证明，莫洛尼鼠白血病病毒（M-MLV）感染与接触3-甲基胆蒽（3-MC）可协同作用，使NIH/3T3小鼠成纤维细胞发生转化。M-MLV似乎能刺激c-myc及某种主要组织相容性复合体（MHC）I类基因的表达。然而，单独的M-MLV感染不足以使这些细胞发生转化。但是，将感染的细胞暴露于3-MC会导致快速的细胞转化，同时转化细胞中c-Ha-ras和H-2K I类MHC基因表达增强。当未感染的NIH/3T3细胞用这种致癌物进行类似处理时，未观察到这种转化。发现由M-MLV和3-MC的这种联合作用转化的细胞克隆在完全具有免疫活性的同种异体BALB/c小鼠中具有高度致瘤性。我们提供的证据表明，这些转化细胞中H-2K基因表达的增强在克服BALB/c同种异体屏障并使肿瘤在这些小鼠中生长方面发挥着重要作用。
