24
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Caenorhabditis elegans as a model for cancer research

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The term cancer describes a group of multifaceted diseases characterized by an intricate pathophysiology. Despite significant advances in the fight against cancer, it remains a key public health concern and burden on societies worldwide. Elucidation of key molecular and cellular mechanisms of oncogenic diseases will facilitate the development of better intervention strategies to counter or prevent tumor development. In vivo and in vitro models have long been used to delineate distinct biological processes involved in cancer such as apoptosis, proliferation, angiogenesis, invasion, metastasis, genome instability, and metabolism. In this review, we introduce Caenorhabditis elegans as an emerging animal model for systematic dissection of the molecular basis of tumorigenesis, focusing on the well-established processes of apoptosis and autophagy. Additionally, we propose that C. elegans can be used to advance our understanding of cancer progression, such as deregulation of energy metabolism, stem cell reprogramming, and host–microflora interactions.

          Related collections

          Most cited references68

          • Record: found
          • Abstract: found
          • Article: not found

          Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009.

          Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic cell death' is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including 'entosis', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor.

            The biochemical properties of beclin 1 suggest a role in two fundamentally important cell biological pathways: autophagy and apoptosis. We show here that beclin 1-/- mutant mice die early in embryogenesis and beclin 1+/- mutant mice suffer from a high incidence of spontaneous tumors. These tumors continue to express wild-type beclin 1 mRNA and protein, establishing that beclin 1 is a haploinsufficient tumor suppressor gene. Beclin 1-/- embryonic stem cells have a severely altered autophagic response, whereas their apoptotic response to serum withdrawal or UV light is normal. These results demonstrate that beclin 1 is a critical component of mammalian autophagy and establish a role for autophagy in tumor suppression. They both provide a biological explanation for recent evidence implicating beclin 1 in human cancer and suggest that mutations in other genes operating in this pathway may contribute to tumor formation through deregulation of autophagy.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Reactive oxygen species in cancer cells: live by the sword, die by the sword.

              Reactive oxygen species and tumor biology are intertwined in a complex web, making it difficult to understand which came first, whether oxidants are required for tumor cell growth, and whether oxidant stress can be exploited therapeutically. Evidence suggests that transformed cells use ROS signals to drive proliferation and other events required for tumor progression. This confers a state of increased basal oxidative stress, making them vulnerable to chemotherapeutic agents that further augment ROS generation or that weaken antioxidant defenses of the cell. In this respect, it appears that tumor cells may die by the same systems they require.
                Bookmark

                Author and article information

                Journal
                Mol Cell Oncol
                Mol Cell Oncol
                KMCO
                Molecular & Cellular Oncology
                Taylor & Francis
                2372-3556
                Apr-Jun 2015
                1 December 2014
                : 2
                : 2
                : e975027
                Affiliations
                [1 ]Institute of Molecular Biology and Biotechnology; Foundation for Research and Technology-Hellas
                [2 ]Department of Basic Sciences; Faculty of Medicine; University of Crete Heraklion ; Crete, Greece
                Author notes
                [†]

                These authors contributed equally.

                [* ]Correspondence to: N. Tavernarakis; Email: tavernarakis@ 123456imbb.forth.gr
                Article
                975027
                10.4161/23723556.2014.975027
                4905018
                27308424
                c05fb895-a802-4796-bca9-7a6561f38e42
                © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

                History
                : 6 August 2014
                : 18 September 2014
                : 18 September 2014
                Page count
                Figures: 3, Tables: 0, References: 99, Pages: 11
                Categories
                Review

                caenorhabditis elegans,cancer,cancer stem cells,cell death,cellular energetics,genome instability,host-microbe interactions,tumor

                Comments

                Comment on this article