Cis-eQTL analysis and functional validation of candidate susceptibility genes for high-grade serous ovarian cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12

AUTHORS

Kate Lawrenson, Qiyuan Li, Siddhartha Kar, Ji-Heui Seo, Jonathan Tyrer, Tassja J. Spindler, Janet Lee, Yibu Chen, Alison Karst, Ronny Drapkin, Katja K. H. Aben, Hoda Anton-Culver, Natalia Antonenkova, Australian Ovarian Cancer Study Group, David Bowtell, Penelope M. Webb, Anna deFazio, Helen Baker, Elisa V. Bandera, Yukie Bean, Matthias W. Beckmann, Andrew Berchuck, Maria Bisogna, Line Bjorge, Natalia Bogdanova, Louise A. Brinton, Angela Brooks-Wilson, Fiona Bruinsma, Ralf Butzow, Ian G. Campbell, Karen Carty, Jenny Chang-Claude, Georgia Chenevix-Trench, Anne Chen, Zhihua Chen, Linda S. Cook, Daniel W. Cramer, Julie M. Cunningham, Cezary Cybulski, Agnieszka Dansonka-Mieszkowska, Joe Dennis, Ed Dicks, Jennifer A. Doherty, Thilo Dörk, Andreas du Bois, Matthias Dürst, Diana Eccles, Douglas T. Easton, Robert P. Edwards, Ursula Eilber, Arif B. Ekici, Peter A. Fasching, Brooke L. Fridley, Yu-Tang Gao, Aleksandra Gentry-Maharaj, Graham G. Giles, Rosalind Glasspool, Ellen L. Goode, Marc T. Goodman, Jacek Grownwald, Patricia Harrington, Philipp Harter, Hanis Nazihah Hasmad, Alexander Hein, Florian Heitz, Michelle A. T. Hildebrandt, Peter Hillemanns, Estrid Hogdall, Claus Hogdall, Satoyo Hosono, Edwin S. Iversen, Anna Jakubowska, Paul James, Allan Jensen, Bu-Tian Ji, Beth Y. Karlan, Susanne Kruger Kjaer, Linda E. Kelemen, Melissa Kellar, Joseph L. Kelley, Lambertus A. Kiemeney, Camilla Krakstad, Jolanta Kupryjanczyk, Diether Lambrechts, Sandrina Lambrechts, Nhu D. Le, Alice W. Lee, Shashi Lele, Arto Leminen, Jenny Lester, Douglas A. Levine, Dong Liang, Jolanta Lissowska, Karen Lu, Jan Lubinski, Lene Lundvall, Leon F. A. G. Massuger, Keitaro Matsuo, Valerie McGuire, John R. McLaughlin, Heli Nevanlinna, Ian McNeish, Usha Menon, Francesmary Modugno, Kirsten B. Moysich, Steven A. Narod, Lotte Nedergaard, Roberta B. Ness, Mat Adenan Noor Azmi, Kunle Odunsi, Sara H. Olson, Irene Orlow, Sandra Orsulic, Rachel Palmieri Weber, Celeste L. Pearce, Tanja Pejovic, Liisa M. Pelttari, Jennifer Permuth-Wey, Catherine M. Phelan, Malcolm C. Pike, Elizabeth M. Poole, Susan J. Ramus, Harvey A. Risch, Barry Rosen, Mary Anne Rossing, Joseph H. Rothstein, Anja Rudolph, Ingo B. Runnebaum, Iwona K. Rzepecka, Helga B. Salvesen, Joellen M. Schildkraut, Ira Schwaab, Thomas A. Sellers, Xiao-Ou Shu, Yurii B. Shvetsov, Nadeem Siddiqui, Weiva Sieh, Honglin Song, Melissa C. Southey, Lara Sucheston, Ingvild L. Tangen, Soo-Hwang Teo, Kathryn L. Terry, Pamela J. Thompson, Agnieszka Timorek, Ya-Yu Tsai, Shelley S. Tworoger, Anne M. van Altena, Els Van Nieuwenhuysen, Ignace Vergote, Robert A. Vierkant, Shan Wang-Gohrke, Christine Walsh, Nicolas Wentzensen, Alice S. Whittemore, Kristine G. Wicklund, Lynne R. Wilkens, Yin-Ling Woo, Xifeng Wu, Anna H. Wu, Hannah Yang, Wei Zheng, Argyrios Ziogas, Alvaro Monteiro, Paul D. Pharoah, Simon A. Gayther, Matthew L. Freedman

ABSTRACT

Genome-wide association studies have reported 11 regions conferring risk of high-grade serous epithelial ovarian cancer (HGSOC). Expression quantitative trait locus (eQTL) analyses can identify candidate susceptibility genes at risk loci. Here we evaluate cis-eQTL associations at 47 regions associated with HGSOC risk (P≤10(-5)). For three cis-eQTL associations (P<1.4 × 10(-3), FDR<0.05) at 1p36 (CDC42), 1p34 (CDCA8) and 2q31 (HOXD9), we evaluate the functional role of each candidate by perturbing expression of each gene in HGSOC precursor cells. Overexpression of HOXD9 increases anchorage-independent growth, shortens population-doubling time and reduces contact inhibition. Chromosome conformation capture identifies an interaction between rs2857532 and the HOXD9 promoter, suggesting this SNP is a leading causal variant. Transcriptomic profiling after HOXD9 overexpression reveals enrichment of HGSOC risk variants within HOXD9 target genes (P=6 × 10(-10) for risk variants (P<10(-4)) within 10 kb of a HOXD9 target gene in ovarian cells), suggesting a broader role for this network in genetic susceptibility to HGSOC. More... »

PAGES

8234

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    6

    Author Affiliations

  • University of Southern California
  • Dana–Farber Cancer Institute
  • University of Cambridge
  • Radboud University Nijmegen Medical Centre
  • University of California, Irvine
  • Peter MacCallum Cancer Centre
  • QIMR Berghofer Medical Research Institute
  • Westmead Hospital
  • Rutgers University
  • Oregon Health & Science University
  • Duke University Hospital
  • Memorial Sloan Kettering Cancer Center
  • University of Bergen
  • Hannover Medical School
  • National Cancer Institute
  • Simon Fraser University
  • Cancer Council Victoria
  • Helsinki University Central Hospital
  • University of Melbourne
  • Beatson West of Scotland Cancer Centre
  • German Cancer Research Center
  • Moffitt Cancer Center
  • University of New Mexico
  • Harvard University
  • Mayo Clinic
  • Pomeranian Medical University
  • Dartmouth College
  • Kliniken Essen-Mitte
  • University of Southampton
  • University of Pittsburgh
  • University of California Los Angeles
  • University of Kansas Medical Center
  • Shanghai Cancer Institute
  • University College London
  • Cedars-Sinai Medical Center
  • The University of Texas MD Anderson Cancer Center
  • University of Copenhagen
  • Aichi Cancer Center
  • Duke University
  • Danish Cancer Society
  • Medical University of South Carolina
  • KU Leuven
  • Universitaire Ziekenhuizen Leuven
  • BC Cancer Agency
  • Roswell Park Cancer Institute
  • Texas Southern University
  • Centrum Onkologii Instytut
  • Kyushu University
  • Stanford University
  • University of Glasgow
  • The University of Texas Health Science Center at Houston
  • Brigham and Women's Hospital
  • Yale University
  • University of Toronto
  • University of Washington
  • Vanderbilt University
  • University of Hawaii at Manoa
  • Glasgow Royal Infirmary
  • University of Ulm
  • Fred Hutchinson Cancer Research Center
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms9234

    DOI

    http://dx.doi.org/10.1038/ncomms9234

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1008734755

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26391404


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    82 schema:description Genome-wide association studies have reported 11 regions conferring risk of high-grade serous epithelial ovarian cancer (HGSOC). Expression quantitative trait locus (eQTL) analyses can identify candidate susceptibility genes at risk loci. Here we evaluate cis-eQTL associations at 47 regions associated with HGSOC risk (P≤10(-5)). For three cis-eQTL associations (P<1.4 × 10(-3), FDR<0.05) at 1p36 (CDC42), 1p34 (CDCA8) and 2q31 (HOXD9), we evaluate the functional role of each candidate by perturbing expression of each gene in HGSOC precursor cells. Overexpression of HOXD9 increases anchorage-independent growth, shortens population-doubling time and reduces contact inhibition. Chromosome conformation capture identifies an interaction between rs2857532 and the HOXD9 promoter, suggesting this SNP is a leading causal variant. Transcriptomic profiling after HOXD9 overexpression reveals enrichment of HGSOC risk variants within HOXD9 target genes (P=6 × 10(-10) for risk variants (P<10(-4)) within 10 kb of a HOXD9 target gene in ovarian cells), suggesting a broader role for this network in genetic susceptibility to HGSOC.
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