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The reverse evolution from multicellularity to unicellularity during carcinogenesis

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  • Han Chen

    (Key Laboratory of Gene Engineering of Ministry of Education, Cooperative Innovation Center for High Performance Computing, College of Ecology and Evolution, Sun Yat-sen University)

  • Fangqin Lin

    (Key Laboratory of Gene Engineering of Ministry of Education, Cooperative Innovation Center for High Performance Computing, College of Ecology and Evolution, Sun Yat-sen University)

  • Ke Xing

    (Key Laboratory of Gene Engineering of Ministry of Education, Cooperative Innovation Center for High Performance Computing, College of Ecology and Evolution, Sun Yat-sen University
    Key Laboratory of Biodiversity Dynamics and Conservation of Guangdong Higher Education Institutes, Sun Yat-Sen University)

  • Xionglei He

    (Key Laboratory of Gene Engineering of Ministry of Education, Cooperative Innovation Center for High Performance Computing, College of Ecology and Evolution, Sun Yat-sen University
    Key Laboratory of Biodiversity Dynamics and Conservation of Guangdong Higher Education Institutes, Sun Yat-Sen University)

Abstract

Theoretical reasoning suggests that cancer may result from a knockdown of the genetic constraints that evolved for the maintenance of metazoan multicellularity. By characterizing the whole-life history of a xenograft tumour, here we show that metastasis is driven by positive selection for general loss-of-function mutations on multicellularity-related genes. Expression analyses reveal mainly downregulation of multicellularity-related genes and an evolving expression profile towards that of embryonic stem cells, the cell type resembling unicellular life in its capacity of unlimited clonal proliferation. Also, the emergence of metazoan multicellularity ~600 Myr ago is accompanied by an elevated birth rate of cancer genes, and there are more loss-of-function tumour suppressors than activated oncogenes in a typical tumour. These data collectively suggest that cancer represents a loss-of-function-driven reverse evolution back to the unicellular ‘ground state’. This cancer evolution model may account for inter-/intratumoural genetic heterogeneity, could explain distant-organ metastases and hold implications for cancer therapy.

Suggested Citation

  • Han Chen & Fangqin Lin & Ke Xing & Xionglei He, 2015. "The reverse evolution from multicellularity to unicellularity during carcinogenesis," Nature Communications, Nature, vol. 6(1), pages 1-10, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7367
    DOI: 10.1038/ncomms7367
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    Cited by:

    1. Anthony Szedlak & Nicholas Smith & Li Liu & Giovanni Paternostro & Carlo Piermarocchi, 2016. "Evolutionary and Topological Properties of Genes and Community Structures in Human Gene Regulatory Networks," PLOS Computational Biology, Public Library of Science, vol. 12(6), pages 1-16, June.

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