Blog
About

  • Record: found
  • Abstract: found
  • Article: found
Is Open Access

Endocannabinoid system as a regulator of tumor cell malignancy – biological pathways and clinical significance

Read this article at

ScienceOpenPublisherPMC
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 endocannabinoid system (ECS) comprises cannabinoid receptors (CBs), endogenous cannabinoids, and enzymes responsible for their synthesis, transport, and degradation of (endo)cannabinoids. To date, two CBs, CB1 and CB2, have been characterized; however, orphan G-protein-coupled receptor GPR55 has been suggested to be the third putative CB. Several different types of cancer present abnormal expression of CBs, as well as other components of ECS, and this has been shown to correlate with the clinical outcome. Although most effects of (endo)cannabinoids are mediated through stimulation of classical CBs, they also interact with several molecules, either prosurvival or proapoptotic molecules. It should be noted that the mode of action of exogenous cannabinoids differs significantly from that of endocannabinoid and results from the studies on their activity both in vivo and in vitro could not be easily compared. This review highlights the main signaling pathways involved in the antitumor activity of cannabinoids and the influence of their activation on cancer cell biology. We also discuss changes in the expression pattern of the ECS in various cancer types that have an impact on disease progression and patient survival. A growing amount of experimental data imply possible exploitation of cannabinoids in cancer therapy.

      Related collections

      Most cited references 146

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

      Autophagy in the pathogenesis of disease.

      Autophagy is a lysosomal degradation pathway that is essential for survival, differentiation, development, and homeostasis. Autophagy principally serves an adaptive role to protect organisms against diverse pathologies, including infections, cancer, neurodegeneration, aging, and heart disease. However, in certain experimental disease settings, the self-cannibalistic or, paradoxically, even the prosurvival functions of autophagy may be deleterious. This Review summarizes recent advances in understanding the physiological functions of autophagy and its possible roles in the causation and prevention of human diseases.
        Bookmark
        • Record: found
        • Abstract: found
        • Article: not found

        Molecular mechanisms and clinical applications of angiogenesis.

        Blood vessels deliver oxygen and nutrients to every part of the body, but also nourish diseases such as cancer. Over the past decade, our understanding of the molecular mechanisms of angiogenesis (blood vessel growth) has increased at an explosive rate and has led to the approval of anti-angiogenic drugs for cancer and eye diseases. So far, hundreds of thousands of patients have benefited from blockers of the angiogenic protein vascular endothelial growth factor, but limited efficacy and resistance remain outstanding problems. Recent preclinical and clinical studies have shown new molecular targets and principles, which may provide avenues for improving the therapeutic benefit from anti-angiogenic strategies.
          Bookmark
          • Record: found
          • Abstract: found
          • Article: not found

          The mammalian unfolded protein response.

          In the endoplasmic reticulum (ER), secretory and transmembrane proteins fold into their native conformation and undergo posttranslational modifications important for their activity and structure. When protein folding in the ER is inhibited, signal transduction pathways, which increase the biosynthetic capacity and decrease the biosynthetic burden of the ER to maintain the homeostasis of this organelle, are activated. These pathways are called the unfolded protein response (UPR). In this review, we briefly summarize principles of protein folding and molecular chaperone function important for a mechanistic understanding of UPR-signaling events. We then discuss mechanisms of signal transduction employed by the UPR in mammals and our current understanding of the remodeling of cellular processes by the UPR. Finally, we summarize data that demonstrate that UPR signaling feeds into decision making in other processes previously thought to be unrelated to ER function, e.g., eukaryotic starvation responses and differentiation programs.
            Bookmark

            Author and article information

            Affiliations
            [1 ]Centre for Innovative Research in Medical and Natural Sciences, Faculty of Medicine
            [2 ]Department of Immunology, Faculty of Medicine, University of Rzeszów, Rzeszów
            [3 ]Postgraduate School of Molecular Medicine, Medical University of Warsaw, Warszawa
            [4 ]Department of Pathophysiology, Medical University of Lublin
            [5 ]Isobolographic Analysis Laboratory, Institute of Agricultural Medicine, Lublin, Poland
            Author notes
            Correspondence: Maria Pyszniak, Centre for Innovative Research in Medical and Natural Sciences, Faculty of Medicine, University of Rzeszów, Warzywna 1a, PL 35-310 Rzeszów, Poland, Email pyszniakmaria@ 123456gmail.com
            Journal
            Onco Targets Ther
            Onco Targets Ther
            OncoTargets and Therapy
            OncoTargets and therapy
            Dove Medical Press
            1178-6930
            2016
            18 July 2016
            : 9
            : 4323-4336
            27486335
            4958360
            10.2147/OTT.S106944
            ott-9-4323
            © 2016 Pyszniak et al. This work is published and licensed by Dove Medical Press Limited

            The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

            Categories
            Review

            Comments

            Comment on this article