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Facilitating replication under stress: an oncogenic function of MYC?

Nature Reviews Cancer volume 9, pages 441–444 (2009)Cite this article

Abstract

Deregulated expression of MYC contributes to the genesis of multiple human tumours. The encoded protein, MYC, functions through the transcriptional regulation of large numbers of target genes. Recent publications show that MYC is closely involved in DNA replication and the checkpoint processes that monitor progress through the S phase, and suggest that limiting replication stress is a key function of this protein. These findings could have considerable implications for our understanding of how MYC transforms cells and which mechanisms protect normal cells from transformation by activated oncogenes.

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Figure 1: Regulation of MYC function by HIF1α and HIF2α proteins in renal carcinoma.
Figure 2: Interactions of MYC with DNA damage signalling pathways.
Figure 3: Role of MYC at origins of DNA replication

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Acknowledgements

The work of the authors' laboratory that is described here was supported by grants from the Deutsche Forschungsgemeinschaft via Transregio 17 (“Ras-dependent pathways in human cancer”) and Research Group 531 (“Chromatin-mediated biological decisions”).

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Authors and Affiliations

  1. Steffi Herold, Barbara Herkert and Martin Eilers are at Theodor-Boveri-Institute, Physiological Chemistry Biocenter Am Hubland, Wrzburg, 97074 Germany.,

    Steffi Herold, Barbara Herkert & Martin Eilers

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Correspondence to Martin Eilers.

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Herold, S., Herkert, B. & Eilers, M. Facilitating replication under stress: an oncogenic function of MYC?. Nat Rev Cancer 9, 441–444 (2009). https://doi.org/10.1038/nrc2640

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