| Literature DB >> 11571630 |
R Jasty1, C van Golen, H J Lin, G Solomon, K Heidelberger, P Polverini, A Opipari, E Feldman, V P Castle.
Abstract
The bcl-2 and c-myc oncogenes cooperate to transform multiple cell types. In the pediatric malignancy NB(2), Bcl-2 is highly expressed. In tumors with a poor prognosis, N-Myc, a protein homologous to c-Myc, is overexpressed as a result of gene amplification. The present study was designed to determine whether Bcl-2 cooperates with N-Myc to bestow a tumorigenic phenotype to neuroblastoma (NB) cells. NB cell lines that at baseline express neither Bcl-2 nor N-Myc were stably transfected to express these gene products. In this model, we found Bcl-2 rescues N-Myc-expressing cells from apoptosis induced by serum withdrawal. Coexpression of Bcl-2 and N-Myc supports growth in low serum conditions and anchorage-independent growth in soft agar. Similarly, in vivo tumorigenic and angiogenic activity was dependent on coexpression. Our data further suggests that the mechanism underlying these changes involves the receptor for insulin growth factor type I (IGF-IR).Entities:
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Year: 2001 PMID： 11571630 PMCID： PMC1505862 DOI： 10.1038/sj.neo.7900171
Source DB: PubMed Journal: Neoplasia ISSN： 1476-5586 Impact factor: 5.715