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      CHD1L: a novel oncogene

      review-article
      Author(s): 1 , , 2 , 1
      Publication date (Electronic):
      Journal: Molecular Cancer
      Publisher: BioMed Central
      Keywords: CHD1L, ALC1, Oncogene, Chr1q21, Amplification, ARHGEF9, SPOCK1, Nur77

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          Abstract

          Comprehensive sequencing efforts have revealed the genomic landscapes of common forms of human cancer and ~ 140 driver genes have been identified, but not all of them have been extensively investigated. CHD1L (chromodomain helicase/ATPase DNA binding protein 1-like gene) or ALC1 (amplified in liver cancer 1) is a newly identified oncogene located at Chr1q21 and it is amplified in many solid tumors. Functional studies of CHD1L in hepatocellular carcinoma and other tumors strongly suggested that its oncogenic role in tumorigenesis is through unleashed cell proliferation, G1/S transition and inhibition of apoptosis. The underlying mechanisms of CHD1L activation may disrupt the cell death program via binding the apoptotic protein Nur77 or through activation of the AKT pathway by up-regulation of CHD1L-mediated target genes (e.g., ARHGEF9, SPOCK1 or TCTP). CHD1L is now considered to be a novel independent biomarker for progression, prognosis and survival in several solid tumors. The accumulated knowledge about its functions will provide a focus to search for targeted treatment in specific subtypes of tumors.

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          Creation of human tumour cells with defined genetic elements.

          W. Hahn, C M Counter, A S Lundberg … (1999)
          During malignant transformation, cancer cells acquire genetic mutations that override the normal mechanisms controlling cellular proliferation. Primary rodent cells are efficiently converted into tumorigenic cells by the coexpression of cooperating oncogenes. However, similar experiments with human cells have consistently failed to yield tumorigenic transformants, indicating a fundamental difference in the biology of human and rodent cells. The few reported successes in the creation of human tumour cells have depended on the use of chemical or physical agents to achieve immortalization, the selection of rare, spontaneously arising immortalized cells, or the use of an entire viral genome. We show here that the ectopic expression of the telomerase catalytic subunit (hTERT) in combination with two oncogenes (the simian virus 40 large-T oncoprotein and an oncogenic allele of H-ras) results in direct tumorigenic conversion of normal human epithelial and fibroblast cells. These results demonstrate that disruption of the intracellular pathways regulated by large-T, oncogenic ras and telomerase suffices to create a human tumor cell.
          Article 0 comments Cited 379 times – based on 0 reviews     Review now
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            Poly(ADP-ribosyl)ation directs recruitment and activation of an ATP-dependent chromatin remodeler.

            Aaron J Gottschalk, Gyula Timinszky, Stephanie E Kong … (2009)
            Posttranslational modifications play a key role in recruiting chromatin remodeling and modifying enzymes to specific regions of chromosomes to modulate chromatin structure. Alc1 (amplified in liver cancer 1), a member of the SNF2 ATPase superfamily with a carboxy-terminal macrodomain, is encoded by an oncogene implicated in the pathogenesis of hepatocellular carcinoma. Here we show that Alc1 interacts transiently with chromatin-associated proteins, including histones and the poly(ADP-ribose) polymerase Parp1. Alc1 ATPase and chromatin remodeling activities are strongly activated by Parp1 and its substrate NAD and require an intact macrodomain capable of binding poly(ADP-ribose). Alc1 is rapidly recruited to nucleosomes in vitro and to chromatin in cells when Parp1 catalyzes PAR synthesis. We propose that poly(ADP-ribosyl)ation of chromatin-associated Parp1 serves as a mechanism for targeting a SNF2 family remodeler to chromatin.
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              Current progress of siRNA/shRNA therapeutics in clinical trials.

              John C Burnett, Katrin Tiemann, John J Rossi (2011)
              Through a mechanism known as RNA interference (RNAi), small interfering RNA (siRNA) molecules can target complementary mRNA strands for degradation, thus specifically inhibiting gene expression. The ability of siRNAs to inhibit gene expression offers a mechanism that can be exploited for novel therapeutics. Indeed, over the past decade, at least 21 siRNA therapeutics have been developed for more than a dozen diseases, including various cancers, viruses, and genetic disorders. Like other biological drugs, RNAi-based therapeutics often require a delivery vehicle to transport them to the targeted cells. Thus, the clinical advancement of numerous siRNA drugs has relied on the development of siRNA carriers, including biodegradable nanoparticles, lipids, bacteria, and attenuated viruses. Most therapies permit systemic delivery of the siRNA drug, while others use ex vivo delivery by autologous cell therapy. Advancements in bioengineering and nanotechnology have led to improved control of delivery and release of some siRNA therapeutics. Likewise, progress in molecular biology has allowed for improved design of the siRNA molecules. Here, we provide an overview of siRNA therapeutics in clinical trials, including their clinical progress, the challenges they have encountered, and the future they hold in the treatment of human diseases. Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
              Article 0 comments Cited 127 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Wen Cheng
                Yun Su
                Feng Xu
                Journal
                Journal ID (nlm-ta): Mol Cancer
                Journal ID (iso-abbrev): Mol. Cancer
                Title: Molecular Cancer
                Publisher: BioMed Central
                ISSN (Electronic): 1476-4598
                Publication date Collection: 2013
                Publication date (Electronic): 21 December 2013
                Volume: 12
                Page: 170
                Affiliations
                [1 ]Department of Urology, Nanjing Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, Jiangsu, P.R. of China
                [2 ]Outpatient department of Eastern Division, First Hospital of Nanjing, Nanjing Medical University, Nanjing, P.R. of China
                Article
                Publisher ID: 1476-4598-12-170
                DOI: 10.1186/1476-4598-12-170
                PMC ID: 3931672
                PubMed ID: 24359616
                SO-VID: c32aa1f8-d5ce-4ca3-903f-4718c4ff69fd
                Copyright © Copyright © 2013 Cheng et al.; licensee BioMed Central Ltd.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 22 August 2013
                Date accepted : 19 December 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: chd1l,alc1,oncogene,chr1q21,amplification,arhgef9,spock1,nur77
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: chd1l, alc1, oncogene, chr1q21, amplification, arhgef9, spock1, nur77

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