Tumorigenicity of hamster and mouse cells transformed by adenovirus types 2 and 5 is not influenced by the level of class I major histocompatibility antigens expressed on the cells.

Abstract

Inbred hamster and mouse cells transformed by the nononcogenic adenovirus (Ad) serotypes, Ad2 and AdS, are nontumorigenic in syngeneic adult animals, while cells from these species transformed by the highly oncogenic Adl2 are tumorigenic in such rodents. By immunoprecipitation and flow cytometry, cells from four of six Ad2-and Ad5-transformed hamster and mouse lines expressed high levels of cell-surface class I major histocompatibility complex (MHC) antigens, while cells from two of these six lines expressed low levels of cell-surface class I MHC antigens. The levels of class I MHC proteins expressed by cells from these latter two lines were comparable to the levels of cell-surface class I MHC proteins expressed by cells from Adl2-transformed hamster and mouse lines. Moreover, an Ad2-transformed line that had become highly oncogenic after in vivo adaptation showed the same high level of MHC expression as the nononcogenic parent. The amounts of class I mRNA, analyzed by RNA blotting, were, in general, consistent with the levels of class I antigens expressed on the surfaces of these cells. These results indicate that there is no correlation between the tumorigenicity in immunocompetent syngeneic adult rodents of Ad2-and Ad5-transformed hamster and mouse cells and the level of class I MHC antigens expressed on the surfaces of these cells. Thus, the expression of different levels of class I MHC proteins does not seem to explain the differences in the oncogenicity between nononcogenic and highly oncogenic human Ad serotypes.Human adenoviruses (Ad) were first shown to be oncogenic in Syrian hamsters by Trentin and coworkers in 1962 (1). Following this discovery, several Ad serotypes were categorized into nononcogenic (Adl, Ad2, Ad5) and highly oncogenic (Adl2, Adl8, Ad3M) groups by their capacity to induce tumors in hamsters and other rodents (2). In spite of the differences in oncogenicity of different Ad

Regulation of p53 mediated transactivation by the β‐subunit of protein kinase CK2

“…p53 not only transactivates gene expression but also can transrepress some genes such as the c‐fos gene [64]. As shown in the present study the influence of the β‐subunit of CK2 seems to be restricted to an influence on the transactivation and not on the transrepression function of p53.…”

Role of p300-family proteins in E1A oncogene induction of cytolytic susceptibility and tumor cell rejection

“…The available data do not support either of these mechanisms. E1A of Ad type 2 or type 5 does not predictably alter MHC class I molecule expression (52,53). Furthermore, some E1A-transfected, NK-susceptible target cells actually express more MHC class I molecules than the NK-resistant cells from which they were derived (6,54).…”

De NovoMethylation of an MHC Class I Transgene Following Transformation with Human Adenoviruses Is Not Correlated with Its Altered Expression

“…The endogenous class I genes and a miniature swine class I transgene (PD1), which is positioned outside of the MHC locus, are generally coregulated. High and low class I expressers were also reported by Haddada et al (1986) among Ad5-transformed cells. The differences observed in mRNA levels raised the possibility that the status of methylation of class I genes varies in individual cell lines and it might affect their expression.…”