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      The metastatic suppressor NDRG1 inhibits EMT, migration and invasion through interaction and promotion of caveolin-1 ubiquitylation in human colorectal cancer cells

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          Abstract

          N-myc downstream-regulated gene 1 (NDRG1) has been reported to act as a key regulatory molecule in tumor progression-related signaling pathways, especially in tumor metastasis. However, the related mechanism has not been fully discovered yet. Herein we demonstrated that the novel molecule of cell migration and invasion, caveolin-1, has direct interaction with NDRG1 in human colorectal cancer (CRC) cells. Moreover, we discovered that NDRG1 reduces caveolin-1 protein expression through promoting its ubiquitylation and subsequent degradation via the proteasome in CRC cells. In addition, caveolin-1 mediates the suppressive function of NDRG1 in epithelial–mesenchymal transition, migration and invasion in vitro and metastasis in vivo. These results help to fulfill the potential mechanisms of NDRG1 in anti-metastatic treatment for human colorectal cancer.

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          Systematic variation in gene expression patterns in human cancer cell lines.

          D T Ross, U Scherf, M B Eisen … (2000)
          We used cDNA microarrays to explore the variation in expression of approximately 8,000 unique genes among the 60 cell lines used in the National Cancer Institute's screen for anti-cancer drugs. Classification of the cell lines based solely on the observed patterns of gene expression revealed a correspondence to the ostensible origins of the tumours from which the cell lines were derived. The consistent relationship between the gene expression patterns and the tissue of origin allowed us to recognize outliers whose previous classification appeared incorrect. Specific features of the gene expression patterns appeared to be related to physiological properties of the cell lines, such as their doubling time in culture, drug metabolism or the interferon response. Comparison of gene expression patterns in the cell lines to those observed in normal breast tissue or in breast tumour specimens revealed features of the expression patterns in the tumours that had recognizable counterparts in specific cell lines, reflecting the tumour, stromal and inflammatory components of the tumour tissue. These results provided a novel molecular characterization of this important group of human cell lines and their relationships to tumours in vivo.
          Article 0 comments Cited 388 times – based on 0 reviews     Review now
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            The multiple faces of caveolae.

            Robert Parton, Kai Simons (2007)
            Caveolae are a highly abundant but enigmatic feature of mammalian cells. They form remarkably stable membrane domains at the plasma membrane but can also function as carriers in the exocytic and endocytic pathways. The apparently diverse functions of caveolae, including mechanosensing and lipid regulation, might be linked to their ability to respond to plasma membrane changes, a property that is dependent on their specialized lipid composition and biophysical properties.
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              PTRF-Cavin, a conserved cytoplasmic protein required for caveola formation and function.

              Michelle M. Hill, Michele Bastiani, Robert Luetterforst … (2008)
              Caveolae are abundant cell-surface organelles involved in lipid regulation and endocytosis. We used comparative proteomics to identify PTRF (also called Cav-p60, Cavin) as a putative caveolar coat protein. PTRF-Cavin selectively associates with mature caveolae at the plasma membrane but not Golgi-localized caveolin. In prostate cancer PC3 cells, and during development of zebrafish notochord, lack of PTRF-Cavin expression correlates with lack of caveolae, and caveolin resides on flat plasma membrane. Expression of PTRF-Cavin in PC3 cells is sufficient to cause formation of caveolae. Knockdown of PTRF-Cavin reduces caveolae density, both in mammalian cells and in the zebrafish. Caveolin remains on the plasma membrane in PTRF-Cavin knockdown cells but exhibits increased lateral mobility and accelerated lysosomal degradation. We conclude that PTRF-Cavin is required for caveola formation and sequestration of mobile caveolin into immobile caveolae.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncogene
                Journal ID (iso-abbrev): Oncogene
                Title: Oncogene
                Publisher: Nature Publishing Group
                ISSN (Print): 0950-9232
                ISSN (Electronic): 1476-5594
                Publication date (Print): 27 July 2017
                Publication date (Electronic): 27 March 2017
                Volume: 36
                Issue: 30
                Pages: 4323-4335
                Affiliations
                [1 ]Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, China
                [2 ]Shanghai Minimally Invasive Surgery Center, Shanghai, China
                [3 ]Department of Gastrointestinal Surgery, Peking University Cancer Hospital and Institute , Beijing, China
                [4 ]Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Division of Gastrointestinal Cancer Translational Research Laboratory, Peking University Cancer Hospital and Institute , Beijing, China
                [5 ]Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine , Shanghai, China
                Author notes
                [* ]Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai 200025, China. E-mail: jingsun1982@ 123456sina.cn or zmhtiger@ 123456yeah.net or mingliang-99@ 123456hotmail.com
                Article
                Publisher Item ID: onc201774
                DOI: 10.1038/onc.2017.74
                PMC ID: 5537633
                PubMed ID: 28346422
                SO-VID: 0abbfa6e-8f61-4983-a725-4d5ca0e64489
                Copyright © Copyright © 2017 The Author(s)
                License:

                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 : 06 February 2016
                Date revision received : 15 January 2017
                Date accepted : 14 February 2017
                Categories
                Subject: Original Article

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

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