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      LSD1 controls metastasis of androgen-independent prostate cancer cells through PXN and LPAR6

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          Abstract

          Lysine-specific demethylase 1 (LSD1) was shown to control gene expression and cell proliferation of androgen-dependent prostate cancer (PCa) cells, whereas the role of LSD1 in androgen-independent metastatic prostate cancer remains elusive. Here, we show that depletion of LSD1 leads to increased migration and invasion of androgen-independent PCa cells. Transcriptome and cistrome analyses reveal that LSD1 regulates expression of lysophosphatidic acid receptor 6 ( LPAR6) and cytoskeletal genes including the focal adhesion adaptor protein paxillin (PXN). Enhanced LPAR6 signalling upon LSD1 depletion promotes migration with concomitant phosphorylation of PXN. In mice LPAR6 overexpression enhances, whereas knockdown of LPAR6 abolishes metastasis of androgen-independent PCa cells. Taken together, we uncover a novel mechanism of how LSD1 controls metastasis and identify LPAR6 as a promising therapeutic target to treat metastatic prostate cancer.

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          Small-sample estimation of negative binomial dispersion, with applications to SAGE data.

          Mark Robinson, Gordon K. Smyth (2008)
          We derive a quantile-adjusted conditional maximum likelihood estimator for the dispersion parameter of the negative binomial distribution and compare its performance, in terms of bias, to various other methods. Our estimation scheme outperforms all other methods in very small samples, typical of those from serial analysis of gene expression studies, the motivating data for this study. The impact of dispersion estimation on hypothesis testing is studied. We derive an "exact" test that outperforms the standard approximate asymptotic tests.
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            FAK-Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly.

            Donna J Webb, Karen Donais, Leanna Whitmore … (2004)
            Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration.
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              CEAS: cis-regulatory element annotation system.

              Hyunjin Shin, Tao Liu, Arjun K Manrai … (2009)
              We present a tool designed to characterize genome-wide protein-DNA interaction patterns from ChIP-chip and ChIP-Seq data. This stand-alone extension of our web application CEAS (cis-regulatory element annotation system) provides summary statistics on ChIP enrichment in important genomic regions such as individual chromosomes, promoters, gene bodies or exons, and infers the genes most likely to be regulated by the binding factor under study. CEAS also enables biologists to visualize the average ChIP enrichment signals over specific genomic regions, particularly allowing observation of continuous and broad ChIP enrichment that might be too subtle to detect from ChIP peaks alone. The CEAS Python package is publicly available at http://liulab.dfci.harvard.edu/CEAS.
              Article 0 comments Cited 236 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncogenesis
                Journal ID (iso-abbrev): Oncogenesis
                Title: Oncogenesis
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2157-9024
                Publication date (Print): October 2014
                Publication date (Electronic): 06 October 2014
                Publication date PMC-release: 1 October 2014
                Volume: 3
                Issue: 10
                Page: e120
                Affiliations
                [1 ]Urologische Klinik und Zentrale Klinische Forschung, Klinikum der Universität Freiburg , Freiburg, Germany
                [2 ]Universität Freiburg, Fakultät für Biologie , Freiburg, Germany
                [3 ]Adolf-Butenandt Institut und Munich Center of Integrated Protein Science (CIPS), Ludwig-Maximilians-Universität München , München, Germany
                [4 ]BIOSS Centre of Biological Signaling Studies, Albert-Ludwigs-University , Freiburg, Germany
                [5 ]Deutsches Konsortium für Translationale Krebsforschung (DKTK), Standort , Freiburg, Germany
                Author notes
                [* ]Urologische Klinik und Zentrale Klinische Forschung, Uniklinik Freiburg, Breisacherstrasse 66 , 79106 Freiburg, Germany. E-mail: roland.schuele@ 123456uniklinik-freiburg.de
                Article
                Publisher Item ID: oncsis201434
                DOI: 10.1038/oncsis.2014.34
                PMC ID: 4216900
                PubMed ID: 25285406
                SO-VID: 6220bd09-9233-4615-9966-fb2cba9e7780
                Copyright © Copyright © 2014 Macmillan Publishers Limited
                License:

                Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

                History
                Date received : 14 May 2014
                Date revision received : 05 August 2014
                Date accepted : 17 August 2014
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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