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A pseudo-meiotic centrosomal function of TEX12 in cancer

S Sandhu, LJ Salmon, JE Hunter, CL Wilson, ND Perkins, N Hunter, OR Davies, View ORCID ProfileUL McClurg
doi: https://doi.org/10.1101/509869
S Sandhu
1Howard Hughes Medical Institute, Department of Microbiology and Molecular Genetics, University of California, Davis, CA 95616, USA.
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LJ Salmon
2Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
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JE Hunter
2Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
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CL Wilson
3Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
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ND Perkins
2Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
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N Hunter
1Howard Hughes Medical Institute, Department of Microbiology and Molecular Genetics, University of California, Davis, CA 95616, USA.
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OR Davies
2Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
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  • For correspondence: Urszula.McClurg@liverpool.ac.uk Owen.Davies@newcastle.ac.uk
UL McClurg
2Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
4Institute for Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, UK.
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  • ORCID record for UL McClurg
  • For correspondence: Urszula.McClurg@liverpool.ac.uk Owen.Davies@newcastle.ac.uk
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Abstract

Cell division by meiosis involves an extraordinary chromosome choreography including pairing, synapsis and crossing over between homologous chromosomes1, 2. The many meiosis-specific genes involved in these processes also constitute a latent toolbox of chromosome remodelling and recombination factors that may be exploited through aberrant expression in cancer3, 4. Here, we report that TEX12, a structural protein involved in meiotic chromosome synapsis5–7, is aberrantly expressed in human cancers, with high TEX12 levels correlating with poor prognosis. We find that TEX12 knock-down causes proliferative failure in multiple cancer cell lines, and confirm its role in the early stages of oncogenesis through murine cancer models. Remarkably, somatically expressed TEX12 localises to centrosomes, leading to altered centrosome number and structure, features associated with cancer development. Further, we identify TEX12 in meiotic centrin-rich bodies, likely precursors of the mitotic centrosome, suggesting that this may represent an additional cellular function of TEX12 in meiosis that has been previously overlooked. Thus, we propose that an otherwise meiotic function of TEX12 in centrosome duplication is responsible for promoting oncogenesis and cellular proliferation in cancer, which may be targeted for novel cancer therapeutics and diagnostics.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted January 08, 2019.
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A pseudo-meiotic centrosomal function of TEX12 in cancer
S Sandhu, LJ Salmon, JE Hunter, CL Wilson, ND Perkins, N Hunter, OR Davies, UL McClurg
bioRxiv 509869; doi: https://doi.org/10.1101/509869
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A pseudo-meiotic centrosomal function of TEX12 in cancer
S Sandhu, LJ Salmon, JE Hunter, CL Wilson, ND Perkins, N Hunter, OR Davies, UL McClurg
bioRxiv 509869; doi: https://doi.org/10.1101/509869

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