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).
journal_name
Neoplasiajournal_title
Neoplasia (New York, N.Y.)authors
Jasty R,van Golen C,Lin HJ,Solomon G,Heidelberger K,Polverini P,Opipari A,Feldman E,Castle VPdoi
10.1038/sj.neo.7900171keywords:
subject
Has Abstractpub_date
2001-07-01 00:00:00pages
304-13issue
4eissn
1522-8002issn
1476-5586journal_volume
3pub_type
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