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      CRISPR/Cas9-mediated gene knockout of NANOG and NANOGP8 decreases the malignant potential of prostate cancer cells

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          Abstract

          NANOG expression in prostate cancer is highly correlated with cancer stem cell characteristics and resistance to androgen deprivation. However, it is not clear whether NANOG or its pseudogenes contribute to the malignant potential of cancer. We established NANOG- and NANOGP8-knockout DU145 prostate cancer cell lines using the CRISPR/Cas9 system. Knockouts of NANOG and NANOGP8 significantly attenuated malignant potential, including sphere formation, anchorage-independent growth, migration capability, and drug resistance, compared to parental DU145 cells. NANOG and NANOGP8 knockout did not inhibit in vitro cell proliferation, but in vivo tumorigenic potential decreased significantly. These phenotypes were recovered in NANOG- and NANOGP8-rescued cell lines. These results indicate that NANOG and NANOGP8 proteins are expressed in prostate cancer cell lines, and NANOG and NANOGP8 equally contribute to the high malignant potential of prostate cancer.

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          NIH Image to ImageJ: 25 years of image analysis.

          Lynda C. Schneider, Wayne S Rasband (2013)
          For the past 25 years NIH Image and ImageJ software have been pioneers as open tools for the analysis of scientific images. We discuss the origins, challenges and solutions of these two programs, and how their history can serve to advise and inform other software projects.
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            A Myc network accounts for similarities between embryonic stem and cancer cell transcription programs.

            Jonghwan Kim, Andrew J. Woo, Jianlin Chu … (2010)
            c-Myc (Myc) is an important transcriptional regulator in embryonic stem (ES) cells, somatic cell reprogramming, and cancer. Here, we identify a Myc-centered regulatory network in ES cells by combining protein-protein and protein-DNA interaction studies and show that Myc interacts with the NuA4 complex, a regulator of ES cell identity. In combination with regulatory network information, we define three ES cell modules (Core, Polycomb, and Myc) and show that the modules are functionally separable, illustrating that the overall ES cell transcription program is composed of distinct units. With these modules as an analytical tool, we have reassessed the hypothesis linking an ES cell signature with cancer or cancer stem cells. We find that the Myc module, independent of the Core module, is active in various cancers and predicts cancer outcome. The apparent similarity of cancer and ES cell signatures reflects, in large part, the pervasive nature of Myc regulatory networks. Copyright © 2010 Elsevier Inc. All rights reserved.
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              Module map of stem cell genes guides creation of epithelial cancer stem cells.

              David J. Wong, Helen Liu, Todd W Ridky … (2008)
              Self-renewal is a hallmark of stem cells and cancer, but existence of a shared stemness program remains controversial. Here, we construct a gene module map to systematically relate transcriptional programs in embryonic stem cells (ESCs), adult tissue stem cells, and human cancers. This map reveals two predominant gene modules that distinguish ESCs and adult tissue stem cells. The ESC-like transcriptional program is activated in diverse human epithelial cancers and strongly predicts metastasis and death. c-Myc, but not other oncogenes, is sufficient to reactivate the ESC-like program in normal and cancer cells. In primary human keratinocytes transformed by Ras and I kappa B alpha, c-Myc increases the fraction of tumor-initiating cells by 150-fold, enabling tumor formation and serial propagation with as few as 500 cells. c-Myc-enhanced tumor initiation is cell-autonomous and independent of genomic instability. Thus, activation of an ESC-like transcriptional program in differentiated adult cells may induce pathologic self-renewal characteristic of cancer stem cells.
              Article 0 comments Cited 246 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 8 September 2015
                Publication date (Electronic): 15 June 2015
                Volume: 6
                Issue: 26
                Pages: 22361-22374
                Affiliations
                1 Division of Gene Therapy Science, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan
                2 Department of Urology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan
                Author notes
                Correspondence to: Keisuke Nimura, nimura@ 123456gts.med.osaka-u.ac.jp
                Article
                DOI: 10.18632/oncotarget.4293
                PMC ID: 4673169
                PubMed ID: 26087476
                SO-VID: f1290de7-1cdf-4066-8e56-1317565ff37a
                Copyright © Copyright: © 2015 Kawamura et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 31 March 2015
                Date accepted : 3 June 2015
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: nanog,nanogp8,gene knockout,crispr/cas9,prostate cancer
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: nanog, nanogp8, gene knockout, crispr/cas9, prostate cancer

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