ArticleNeoplasia (New York, N.Y.)
Bcl-2 and M-Myc coexpression increases IGF-IR and features of malignant growth in neuroblastoma cell lines.
Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Inhibition of N-myc expression sensitizes human neuroblastoma IMR-32 cells expressing caspase-8 to TRAIL.Cell proliferation · 2019Article
- Cell type-dependent ROS and mitophagy response leads to apoptosis or necroptosis in neuroblastoma.Oncogene · 2016Article
- Exploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy Combination.Cancer cell · 2016Article
- Quantitative phosphoproteomic analysis identifies activation of the RET and IGF-1R/IR signaling pathways in neuroblastoma.PloS one · 2013Article
- BET inhibition silences expression of MYCN and BCL2 and induces cytotoxicity in neuroblastoma tumor models.PloS one · 2013Article
- Pharmacokinetically guided phase 1 trial of the IGF-1 receptor antagonist RG1507 in children with recurrent or refractory solid tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Article
- N-myc augments death and attenuates protective effects of Bcl-2 in trophically stressed neuroblastoma cells.Oncogene · 2008Article
- Antisense bcl-2 transfection up-regulates anti-apoptotic and anti-oxidant thioredoxin in neuroblastoma cells.Journal of neuro-oncology · 2005Article
- N-Myc overexpression leads to decreased beta1 integrin expression and increased apoptosis in human neuroblastoma cells.Oncogene · 2003Article
- N-Myc and Bcl-2 coexpression induces MMP-2 secretion and activation in human neuroblastoma cells.Oncogene · 2002Article
- Integrin expression regulates neuroblastoma attachment and migration.Neoplasia (New York, N.Y.)Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
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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).
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