Bcl-2 and N-Myc Coexpression Increases IGF-IR and Features of Malignant Growth in Neuroblastoma Cell Lines
作者： Rama Jasty , Cynthia {ptvan} Golen , Huey-Jen Lin , Gabe Solomon , Kathleen Heidelberger
关键词: Cell culture 、 Cancer research 、 Neuroblastoma 、 Fetal bovine serum 、 N-Myc 、 Transfection 、 Cell type 、 Molecular biology 、 Growth factor 、 Insulin-like growth factor 1 receptor 、 Biology
摘要: Abstract The bcl-2 and c-myc oncogenes cooperate to transform multiple cell types. In the pediatric malignancy NB 2 , Bcl2 is highly expressed. tumors with a poor prognosis, N-Myc, protein homologous c-Myc, overexpressed as result of gene amplification. present study was designed determine whether Bcl-2 cooperates N-Myc bestow tumorigenic phenotype neuroblastoma (NB) cells. lines that at baseline express neither nor were stably transfected these products. this model, we found rescues N-Myc-expressing cells from apoptosis induced by serum withdrawal. Coexpression supports growth in low conditions anchorage-independent soft agar. Similarly, vivo angiogenic activity dependent on coexpression. Our data further suggests mechanism underlying changes involves receptor for insulin factor type I (IGF-IR).
core.ac.uk
nature.com
sci-hub.se 参考文章(45)
Valerie P. Castle, Mukund Dole, Gabriel Nuñez, Kathleen P. Heidelberger, Judith Bromberg, Xianglan Ou, Expression of the apoptosis-suppressing protein bcl-2, in neuroblastoma is associated with unfavorable histology and N-myc amplification. American Journal of Pathology. ,vol. 143, pp. 1543- 1550 ,(1993)
S. Krajewski, J. C. Reed, J. Chatten, M. Hanada, Immunohistochemical analysis of the Bcl-2 oncoprotein in human neuroblastomas. Comparisons with tumor cell differentiation and N-Myc protein. Laboratory Investigation. ,vol. 72, pp. 42- 54 ,(1995)
Fahl We, Boeckman Fa, Brondyk Wh, N-myc oncogene enhances mitogenic responsiveness of diploid human fibroblasts to growth factors but fails to immortalize. Oncogene. ,vol. 6, pp. 1269- ,(1991)
Luke Whitesell, Anne Fritz, Thomas Turbyville, Xiangdang Liu, Inhibition of Insulin-like Growth Factor I Receptor Expression in Neuroblastoma Cells Induces the Regression of Established Tumors in Mice Cancer Research. ,vol. 58, pp. 5432- 5438 ,(1998)
Jonathan Maybaum, Valerie P. Castle, Audrea K. Merchant, Mukund Dole, Craig A. Bloch, Christopher K. Rode, Gabriel Nuñez, Bcl-2 inhibits chemotherapy-induced apoptosis in neuroblastoma. Cancer Research. ,vol. 54, pp. 3253- 3259 ,(1994)
Babajko S, Mohseni-Zadeh S, de Gallé B, Chambéry D, N-myc regulation of type I insulin-like growth factor receptor in a human neuroblastoma cell line Cancer Research. ,vol. 59, pp. 2898- 2902 ,(1999)
Peter J. Houghton, Tadashi Sawada, Shinji Akioka, Hajime Hosoi, Takafumi Matsumura, Akiko Misawa, Takuma Shikata, Akiko Arimoto, N-Myc Induction Stimulated by Insulin-like Growth Factor I through Mitogen-activated Protein Kinase Signaling Pathway in Human Neuroblastoma Cells Cancer Research. ,vol. 60, pp. 64- 69 ,(2000)
D Meitar, S E Crawford, A W Rademaker, S L Cohn, Tumor angiogenesis correlates with metastatic disease, N-myc amplification, and poor outcome in human neuroblastoma. Journal of Clinical Oncology. ,vol. 14, pp. 405- 414 ,(1996) , 10.1200/JCO.1996.14.2.405
David G. Poplack, Philip A. Pizzo, Principles and Practice of Pediatric Oncology ,(1989)
Cynthia M. Van Golen, Eva L. Feldman, Insulin-like growth factor I is the key growth factor in serum that protects neuroblastoma cells from hyperosmotic-induced apoptosis. Journal of Cellular Physiology. ,vol. 182, pp. 24- 32 ,(2000) , 10.1002/(SICI)1097-4652(200001)182:1<24::AID-JCP3>3.0.CO;2-6