N-Myc Shares Cellular Functions with c-Myc

Aubry, Stéphane; Charron, Jean
June 2000
DNA & Cell Biology;Jun2000, Vol. 19 Issue 6, p353
Academic Journal
N- Myc is a member of the myc family of proto-oncogenes involved in initiation and progression of tumors. While c-MYC, the most characterized member of the family, is well known for its role in cellular proliferation and apoptosis, the function of N-MYC in differentiation and proliferation remains unclear. N- Myc mutant mice present a phenotype more consistent with a role of N-MYC protein in proliferation of precursor populations than in differentiation per se . Recent studies have also shown that N-MYC can enhance apoptosis and shorten the G[sub 1] phase of the cell cycle. However, the role of N-MYC in instigating cell-cycle progression has not been clearly demonstrated. Here, we demonstrate that overexpression of N- myc or activation of inducible N-MYC proteins is sufficient to induce apoptosis in serum-starved fibroblast cells, an effect that can be counteracted by overexpression of Bcl-2 . Moreover, N-MYC can induce the reentry of quiescent cells into the cell cycle even in the absence of external stimuli. These results indicate that N-MYC and c-MYC share many properties, supporting the model that MYC-specific roles during embryonic development are mediated, at least in part, via their specific profile of expression rather than by their different protein functions.


Related Articles

  • STK38 is a critical upstream regulator of MYC's oncogenic activity in human B-cell lymphoma. Bisikirska, B C; Adam, S J; Alvarez, M J; Rajbhandari, P; Cox, R; Lefebvre, C; Wang, K; Rieckhof, G E; Felsher, D W; Califano, A // Oncogene;11/7/2013, Vol. 32 Issue 45, p5283 

    The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. Besides constituting a formidable therapeutic target, MYC also has an essential function in normal physiology, thus creating the need for...

  • MicroRNA-155 controls affinity-based selection by protecting c-MYC+ B cells from apoptosis. Rinako Nakagawa; Leyland, Rebecca; Meyer-Hermann, Michael; Dong Lu; Turner, Martin; Arbore, Ciuseppina; Tri Ciang Phan; Brink, Robert; Vigorito, Elena; Nakagawa, Rinako; Lu, Dong; Arbore, Giuseppina; Phan, Tri Giang // Journal of Clinical Investigation;Jan2016, Vol. 126 Issue 1, p377 

    The production of high-affinity antibodies by B cells is essential for pathogen clearance. Antibody affinity for antigen is increased through the affinity maturation in germinal centers (GCs). This is an iterative process in which B cells cycle between proliferation coupled with the acquisition...

  • Myc deletion rescues Apc deficiency in the small intestine. Sansom, Owen J.; Meniel, Valerie S.; Muncan, Vanesa; Phesse, Toby J.; Wilkins, Julie A.; Reed, Karen R.; Vass, J. Keith; Athineos, Dimitris; Clevers, Hans; Clarke, Alan R. // Nature;4/5/2007, Vol. 446 Issue 7136, p676 

    The APC gene encodes the adenomatous polyposis coli tumour suppressor protein, germline mutation of which characterizes familial adenomatous polyposis (FAP), an autosomal intestinal cancer syndrome. Inactivation of APC is also recognized as the key early event in the development of sporadic...

  • Regulation of c-myc stability by selective stress conditions and by MEKK1 requires aa 127 - 189 of c-myc. Alarcon-Vargas, Dania; Tansey, William P.; Ronai, Ze'ev // Oncogene;6/27/2002, Vol. 21 Issue 28, p4384 

    Presents information on a study which examined the regulation of c-myc protein stability and identify domains of c-myc that are important for its stabilization in response to stress kinases activated following selective stress conditions. Function of the c-myc protooncogene in cellular...

  • Differential roles of JNK and Smad2 signaling pathways in the inhibition of c-Myc-induced cell death by TGF-β. Mazars, Anne; Tournigand, Christophe; Mollat, Patrick; Prunier, Céline; Ferrand, Nathalie; Bourgeade, Marie-Françoise; Gespach, Christian; Atfi, Azeddine // Oncogene;3/2/2000, Vol. 19 Issue 10, p1277 

    The transforming growth factor beta (TGF-β) plays an important role in constraining cellular proliferation, but it is also a potent inducer of programmed cell death or apoptosis. Here, we demonstrate that TGF-β can have an opposite effect, acting as a survival factor to prevent...

  • The opposing roles of the Akt and c-Myc signalling pathways in survival from CD95-mediated apoptosis. Rohn, Jennifer L; Hueber, Anne-Odile; McCarthy, Nicola J; Lyon, Debbie; Navarro, Paloma; Burgering, Boudewijn M Th; Evan, Gerard I // Oncogene;12/3/98, Vol. 17 Issue 22, p2811 

    Expression of the proto-oncogene c-myc stimulates cell proliferation in the presence of the appropriate survival factors and triggers apoptosis in their absence; this dual capacity ensures that cell growth is restricted to the correct paracrine environment and is thereby strictly controlled....

  • Sensitivity to myc-induced apoptosis is retained in spontaneous and transplanted lymphomas of CD2-mycERTM mice. Blyth, Karen; Stewart, Monica; Bell, Margaret; James, Clarwyn; Evan, Gerard; Neil, James C; Cameron, Ewan R // Oncogene;2/10/2000, Vol. 19 Issue 6, p773 

    To study the effects of the Myc oncoprotein in a regulatable in vivo system, we generated lines of transgenic mice in which a tamoxifen inducible Myc fusion protein (c-mycERTM) is expressed under the control of the CD2 locus control region. Activation of the Myc oncoprotein resulted in both...

  • Inhibition of Myc-dependent apoptosis by eukaryotic translation initiation factor 4E requires cyclin D1. Tan, Annie; Bitterman, Peter; Sonenberg, Nahum; Peterson, Mark; Polunovsky, Vitaly // Oncogene;3/9/2000, Vol. 19 Issue 11, p1437 

    Ectopically expressed eukaryotic translation initiation factor 4E (eIF4E) stimulates cell proliferation, suppresses apoptosis in growth factor restricted cells, and induces malignant transformation in primary rodent fibroblasts when coexpressed with protooncogene myc. We report here that eIF4E...

  • Cdc25 cell-cycle phosphatase as a target of c-myc. Galaktionov, Konstantin; Xiaocun Chen // Nature;8/8/1996, Vol. 382 Issue 6591, p511 

    Looks at a study which indicates that the proto-oncogene cdc25A is a physiologically relevant target of c-myc (Myc). Myc as a member of a family of related genes implicated in the control of normal cell proliferation and the induction of neoplasia; C-myc protein being a transcription factor...


Read the Article


Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics