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BAZ2A (TIP5) is involved in epigenetic alterations in prostate cancer and its overexpression predicts disease recurrence.

  • Gu L 1] Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany. [2] Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Frommel SC 1] Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Zurich, Switzerland. [2] Molecular Life Science Program, Life Science Zurich Graduate School, University of Zurich, Zurich, Switzerland.
  • Oakes CC Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Simon R Institute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • Grupp K Institute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • Gerig CY Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Zurich, Switzerland.
  • Bär D Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Zurich, Switzerland.
  • Robinson MD 1] Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. [2] Swiss Institute of Bioinformatics (SIB), University of Zurich, Zurich, Switzerland.
  • Baer C Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Weiss M Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Gu Z Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Schapira M Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
  • Kuner R Unit of Cancer Genome Research, German Cancer Research Center (DKFZ) and National Center of Tumour Diseases, Heidelberg, Germany.
  • Sültmann H Unit of Cancer Genome Research, German Cancer Research Center (DKFZ) and National Center of Tumour Diseases, Heidelberg, Germany.
  • Provenzano M Oncology Research Unit, Division of Urology, University Hospital of Zurich, Zurich, Switzerland.
  • Yaspo ML Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Brors B Genome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
  • Korbel J Martini Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • Schlomm T Institute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • Sauter G 1] Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany. [2] Department for Bioinformatics and Functional Genomics, Institute for Pharmacy and Molecular Biotechnology (IPMB) and BioQuant, Heidelberg University, Heidelberg, Germany.
  • Eils R Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Plass C Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Zurich, Switzerland.
  • Santoro R
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  • 2014-12-09
Published in:
  • Nature genetics. - 2015
Adenocarcinoma
Biomarkers, Tumor
Cell Division
Cell Line, Tumor
Chromosomal Proteins, Non-Histone
CpG Islands
DNA Methylation
Enhancer of Zeste Homolog 2 Protein
Epigenetic Repression
Follow-Up Studies
Gene Expression Regulation, Neoplastic
Humans
Male
Neoplasm Invasiveness
Neoplasm Metastasis
Neoplasm Proteins
Polycomb Repressive Complex 2
Prognosis
Prostatic Neoplasms
Protein Interaction Mapping
RNA, Neoplasm
RNA, Ribosomal
Up-Regulation
English Prostate cancer is driven by a combination of genetic and/or epigenetic alterations. Epigenetic alterations are frequently observed in all human cancers, yet how aberrant epigenetic signatures are established is poorly understood. Here we show that the gene encoding BAZ2A (TIP5), a factor previously implicated in epigenetic rRNA gene silencing, is overexpressed in prostate cancer and is paradoxically involved in maintaining prostate cancer cell growth, a feature specific to cancer cells. BAZ2A regulates numerous protein-coding genes and directly interacts with EZH2 to maintain epigenetic silencing at genes repressed in metastasis. BAZ2A overexpression is tightly associated with a molecular subtype displaying a CpG island methylator phenotype (CIMP). Finally, high BAZ2A levels serve as an independent predictor of biochemical recurrence in a cohort of 7,682 individuals with prostate cancer. This work identifies a new aberrant role for the epigenetic regulator BAZ2A, which can also serve as a useful marker for metastatic potential in prostate cancer.
Language
  • English
Open access status
green
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/147111
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