Proteome-wide discovery of mislocated proteins in cancer

  1. Bonghee Lee3,4,9
  1. 1Department of Biomedical Informatics, Ajou University School of Medicine, Suwon 443-749, Korea;
  2. 2Department of Biomedical Sciences, Graduate School, Ajou University, Suwon 443-749, Korea;
  3. 3Center for Genomics and Proteomics, Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, Incheon 406-840, Korea;
  4. 4Department of Anatomy and Cell Biology, Gachon University Graduate School of Medicine, Incheon 406-799, Korea;
  5. 5Departments of Medicine and Bioengineering, University of California San Diego, La Jolla, California 92093, USA;
  6. 6Cellular Systems Modeling Team and Cellular Informatics Laboratory, RIKEN Advanced Science Institute, Wako-shi, Saitama 351-0198, Japan;
  7. 7Department of Neurosurgery, Ischemic/Hypoxic Disease Institute, Cancer Research Institute, Seoul National University College of Medicine, Seoul 110-744, Korea
    1. 8 These authors contributed equally to this work.

    Abstract

    Several studies have sought systematically to identify protein subcellular locations, but an even larger task is to map which of these proteins conditionally relocates in disease (the mislocalizome). Here, we report an integrative computational framework for mapping conditional location and mislocation of proteins on a proteome-wide scale, called a conditional location predictor (CoLP). Using CoLP, we mapped the locations of over 10,000 proteins in normal human brain and in glioma. The prediction showed 0.9 accuracy using 100 location tests of 20 randomly selected proteins. Of the 10,000 proteins, over 150 have a strong likelihood of mislocation under glioma, which is striking considering that few mislocation events have been identified in this disease previously. Using immunofluorescence and Western blotting in both primary cells and tissues, we successfully experimentally confirmed 15 mislocations. The most common type of mislocation occurs between the endoplasmic reticulum and the nucleus; for example, for RNF138, TLX3, and NFRKB. In particular, we found that the gene for the mislocating protein GFRA4 had a nonsynonymous point mutation in exon 2. Moreover, redirection of GFRA4 to its normal location, the plasma membrane, led to marked reductions in phospho-STAT3 and proliferation of glioma cells. This framework has the potential to track changes in protein location in many human diseases.

    Footnotes

    • 9 Corresponding authors

      E-mail kiylee{at}ajou.ac.kr

      E-mail bhlee{at}gachon.ac.kr

    • [Supplemental material is available for this article.]

    • Article published online before print. Article, supplemental material, and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.155499.113.

    • Received January 29, 2013.
    • Accepted May 6, 2013.

    This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.

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