This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jelinek, T Articles by Graham, F L Search for Related Content PubMed PubMed Citation Articles by Jelinek, T Articles by Graham, F L

 Previous Article  |  Next Article 

J Virol. 1994 February; 68(2): 888-896

Tumorigenicity of adenovirus-transformed rodent cells is influenced by at least two regions of adenovirus type 12 early region 1A.

Department of Biology, McMaster University, Hamilton, Ontario, Canada.

ABSTRACT

Chimeric adenovirus type 5 (Ad5)/Ad12 early region 1A (E1A) genes were used to transform primary baby rat kidney cells in cooperation with Ad12 E1B, and the resulting cell lines were assayed for tumorigenicity in syngeneic rats. It was found that lines were nontumorigenic when transformed by hybrid E1A genes consisting of the amino-terminal 80 amino acids from Ad12 including conserved region 1 (CR1), with the remaining portion from Ad5. In contrast, cell lines transformed by hybrids containing Ad12 E1A sequences from the amino terminus to the leftmost border of CR3 or beyond were tumorigenic. To extend these results, sequences spanning CR2 and CR3 of Ad5 E1A were replaced with the homologous regions of Ad12 E1A and additional transformed cell lines were established. These lines were weakly-to-moderately tumorigenic, suggesting that Ad12 E1A sequences between CR2 and CR3 may be involved in tumorigenicity but are not the sole factors influencing it. Interestingly, examination of an E1A sequence alignment indicated that the region between CR2 and CR3 of Ad12 E1A is also conserved in the corresponding sequence of simian adenovirus type 7, which, like Ad12, is highly oncogenic. This region is characterized by the presence of a stretch of several alanine residues and is similar to a motif present in a number of proteins with transcriptional repression activity. The possibility that this region may influence tumorigenicity by means of a transcriptional regulatory mechanism is discussed.

This article has been cited by other articles:

• Kosulin, K., Haberler, C., Hainfellner, J. A., Amann, G., Lang, S., Lion, T. (2007). Investigation of Adenovirus Occurrence in Pediatric Tumor Entities. J. Virol. 81: 7629-7635 [Abstract] [Full Text]  
• Avvakumov, N., Wheeler, R., D'Halluin, J. C., Mymryk, J. S. (2002). Comparative Sequence Analysis of the Largest E1A Proteins of Human and Simian Adenoviruses. J. Virol. 76: 7968-7975 [Abstract] [Full Text]  
• Hou, S., Guan, H., Ricciardi, R. P. (2002). In Adenovirus Type 12 Tumorigenic Cells, Major Histocompatibility Complex Class I Transcription Shutoff Is Overcome by Induction of NF-{kappa}B and Relief of COUP-TFII Repression. J. Virol. 76: 3212-3220 [Abstract] [Full Text]  
• Thomas, D. L., Shin, S., Jiang, B. H., Vogel, H., Ross, M. A., Kaplitt, M., Shenk, T. E., Javier, R. T. (1999). Early Region 1 Transforming Functions Are Dispensable for Mammary Tumorigenesis by Human Adenovirus Type 9. J. Virol. 73: 3071-3079 [Abstract] [Full Text]  
• Kushner, D. B., Ricciardi, R. P. (1999). Reduced Phosphorylation of p50 Is Responsible for Diminished NF-kappa B Binding to the Major Histocompatibility Complex Class I Enhancer in Adenovirus Type 12-Transformed Cells. Mol. Cell. Biol. 19: 2169-2179 [Abstract] [Full Text]  
• Brockmann, D., Bury, C., Kröner, G., Kirch, H.-C., Esche, H. (1995). Repression of the c-Jun trans-Activation Function by the Adenovirus Type 12 E1A 52R Protein Correlates with the Inhibition of Phosphorylation of the c-Jun Activation Domain. J. Biol. Chem. 270: 10754-10763 [Abstract] [Full Text]