22
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      RKIP: A Key Regulator in Tumor Metastasis Initiation and Resistance to Apoptosis: Therapeutic Targeting and Impact

      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

          RAF-kinase inhibitor protein (RKIP) is a well-established tumor suppressor that is frequently downregulated in a plethora of solid and hematological malignancies. RKIP exerts antimetastatic and pro-apoptotic properties in cancer cells, via modulation of signaling pathways and gene products involved in tumor survival and spread. Here we review the contribution of RKIP in the regulation of early metastatic steps such as epithelial–mesenchymal transition (EMT), migration, and invasion, as well as in tumor sensitivity to conventional therapeutics and immuno-mediated cytotoxicity. We further provide updated justification for targeting RKIP as a strategy to overcome tumor chemo/immuno-resistance and suppress metastasis, through the use of agents able to modulate RKIP expression in cancer cells.

          Related collections

          Most cited references222

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

          Epithelial-mesenchymal transitions: twist in development and metastasis.

          Epithelial-mesenchymal transitions (EMT) are vital for morphogenesis during embryonic development and are also implicated in the conversion of early stage tumors into invasive malignancies. Several key inducers of EMT are transcription factors that repress E-cadherin expression. A recent report in Cell (Yang et al., 2004) adds Twist to this list and links EMT to the ability of breast cancer cells to enter the circulation and seed metastases.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Notch signalling in solid tumours: a little bit of everything but not all the time.

            The discovery of Notch in Drosophila melanogaster nearly a century ago opened the door to an ever-widening understanding of cellular processes that are controlled or influenced by Notch signalling. As would be expected with such a pleiotropic pathway, the deregulation of Notch signalling leads to several pathological conditions, including cancer. A role for Notch is well established in haematological malignancies, and more recent studies have provided evidence for the importance of Notch activity in solid tumours. As it is thought to act as an oncogene in some cancers but as a tumour suppressor in others, the role of Notch in solid tumours seems to be highly context dependent.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Coordinating ERK/MAPK signalling through scaffolds and inhibitors.

              The pathway from Ras through Raf and MEK (MAPK and ERK kinase) to ERK/MAPK (extracellular signal-regulated kinase/mitogen-activated protein kinase) regulates many fundamental cellular processes. Recently, a number of scaffolding proteins and endogenous inhibitors have been identified, and their important roles in regulating signalling through this pathway are now emerging. Some scaffolds augment the signal flux, but also mediate crosstalk with other pathways; certain adaptors target MEK-ERK/MAPK complexes to subcellular localizations; others provide regulated inhibition. Computational modelling indicates that, together, these modulators can determine the dynamic biological behaviour of the pathway.
                Bookmark

                Author and article information

                Journal
                Cancers (Basel)
                Cancers (Basel)
                cancers
                Cancers
                MDPI
                2072-6694
                24 August 2018
                September 2018
                : 10
                : 9
                : 287
                Affiliations
                [1 ]Department of Life Sciences, School of Sciences, European University Cyprus, 2404 Nicosia, Cyprus; a.zaravinos@ 123456euc.ac.cy
                [2 ]Centre for Risk and Decision Sciences (CERIDES), 2404 Nicosia, Cyprus
                [3 ]Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA; bbonavida@ 123456mednet.ucla.edu
                [4 ]Laboratory of Pharmacology, Medical School, Democritus University of Thrace, 68100 Alexandroupolis, Greece; achatzak@ 123456med.duth.gr
                [5 ]Division of Surgical Oncology, School of Medicine, University of Crete, Heraklion, 71500 Crete, Greece
                Author notes
                [* ]Correspondence: vbaritak@ 123456gmail.com ; Tel.: +30-2810-394727
                Author information
                https://orcid.org/0000-0003-4625-5562
                Article
                cancers-10-00287
                10.3390/cancers10090287
                6162400
                30149591
                360ae472-c4a8-4971-8cf0-6bb4ae8c20c2
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 20 July 2018
                : 18 August 2018
                Categories
                Review

                rkip,cancer,resistance,metastasis,emt,therapy
                rkip, cancer, resistance, metastasis, emt, therapy

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content189

                Cited by16

                Most referenced authors3,248