c-Myc and cancer metabolism - PubMed (original) (raw)

c-Myc and cancer metabolism

Donald M Miller et al. Clin Cancer Res. 2012.

Abstract

The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a "master regulator" which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the increased need for nucleic acids, proteins, and lipids necessary for rapid cellular proliferation. At the same time, c-Myc overexpression results in coordinated changes in level of expression of gene families which result in increased cellular proliferation. This interesting duality of c-Myc effects places it in the mainstream of transformational changes and gives it a very important role in regulating the "transformed phenotype." The effects induced by c-Myc can occur either as a "primary oncogene" which is activated by amplification or translocation or as a downstream effect of other activated oncogenes. In either case, it appears that c-Myc plays a central role in sustaining the changes which occur with transformation. Although efforts to use c-Myc as a therapeutic target have been quite frustrating, it appears that this may change in the next few years.

©2012 AACR

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Conflict of interest statement

Dr. Miller is on the Board of Directors of Advanced Cancer Therapeutics; All other authors declare no potential conflict of interest.

Figures

Figure 1

Figure 1

Diagram of Myc effects in transformed cells. There are a wide variety of downstream pathways which are both positively and negatively regulated by Myc expression.

Figure 2

Figure 2

Pleiotropic Effects of c-Myc Expression. The c-myc gene has a variety of molecular and cellular effects (which are closely related). These effects result from myc-mediated changes in large gene families which drive cellular functions. Microarray studies have shown that these changes occur in concert and have major effects on cellular function.

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References

    1. Morrish F, Neretti N, Sedivy JM, Hockenbery DM. The oncogene c-Myc coordinates regulation of metabolic networks to enable rapid cell cycle entry. Cell Cycle. 2008;7:1054–1066. - PMC - PubMed
    1. Wolfer A, Ramaswamy S. MYC and metastasis. Cancer Res. 2011;71:2034–2037. - PMC - PubMed
    1. Meyer N, Penn LZ. Reflecting on 25 years with MYC. Nat Rev Cancer. 2008;8:976–990. - PubMed
    1. Levens D. You Don't Muck with MYC. Genes Cancer. 2010;1:547–554. - PMC - PubMed
    1. Lombardi L, Newcomb EW, Dalla-Favera R. Pathogenesis of Burkitt lymphoma: expression of an activated c-myc oncogene causes the tumorigenic conversion of EBV-infected human B lymphoblasts. Cell. 1987;49:161–170. - PubMed

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