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      Anti-Inflammatory Drugs as Anticancer Agents

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          Abstract

          Inflammation is strictly associated with cancer and plays a key role in tumor development and progression. Several epidemiological studies have demonstrated that inflammation can predispose to tumors, therefore targeting inflammation and the molecules involved in the inflammatory process could represent a good strategy for cancer prevention and therapy. In the past, several clinical studies have demonstrated that many anti-inflammatory agents, including non-steroidal anti-inflammatory drugs (NSAIDs), are able to interfere with the tumor microenvironment by reducing cell migration and increasing apoptosis and chemo-sensitivity. This review focuses on the link between inflammation and cancer by describing the anti-inflammatory agents used in cancer therapy, and their mechanisms of action, emphasizing the use of novel anti-inflammatory agents with significant anticancer activity.

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          Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes.

          Olivier Micheau, Jurg Tschopp (2003)
          Apoptosis induced by TNF-receptor I (TNFR1) is thought to proceed via recruitment of the adaptor FADD and caspase-8 to the receptor complex. TNFR1 signaling is also known to activate the transcription factor NF-kappa B and promote survival. The mechanism by which this decision between cell death and survival is arbitrated is not clear. We report that TNFR1-induced apoptosis involves two sequential signaling complexes. The initial plasma membrane bound complex (complex I) consists of TNFR1, the adaptor TRADD, the kinase RIP1, and TRAF2 and rapidly signals activation of NF-kappa B. In a second step, TRADD and RIP1 associate with FADD and caspase-8, forming a cytoplasmic complex (complex II). When NF-kappa B is activated by complex I, complex II harbors the caspase-8 inhibitor FLIP(L) and the cell survives. Thus, TNFR1-mediated-signal transduction includes a checkpoint, resulting in cell death (via complex II) in instances where the initial signal (via complex I, NF-kappa B) fails to be activated.
          Article 0 comments Cited 717 times – based on 0 reviews     Review now
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            Mitogen-activated protein kinases in innate immunity.

            J. Simon C. Arthur, Steven C Ley (2013)
            Following pathogen infection or tissue damage, the stimulation of pattern recognition receptors on the cell surface and in the cytoplasm of innate immune cells activates members of each of the major mitogen-activated protein kinase (MAPK) subfamilies--the extracellular signal-regulated kinase (ERK), p38 and Jun N-terminal kinase (JNK) subfamilies. In conjunction with the activation of nuclear factor-κB and interferon-regulatory factor transcription factors, MAPK activation induces the expression of multiple genes that together regulate the inflammatory response. In this Review, we discuss our current knowledge about the regulation and the function of MAPKs in innate immunity, as well as the importance of negative feedback loops in limiting MAPK activity to prevent host tissue damage. We also examine how pathogens have evolved complex mechanisms to manipulate MAPK activation to increase their virulence. Finally, we consider the potential of the pharmacological targeting of MAPK pathways to treat autoimmune and inflammatory diseases.
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              Phosphorylation of NF-kappaB and IkappaB proteins: implications in cancer and inflammation.

              Patrick Viatour, Marie-Paule Merville, Vincent Bours … (2005)
              Nuclear factor-kappaB (NF-kappaB) is a transcription factor that has crucial roles in inflammation, immunity, cell proliferation and apoptosis. Activation of NF-kappaB mainly occurs via IkappaB kinase (IKK)-mediated phosphorylation of inhibitory molecules, including IkappaBalpha. Optimal induction of NF-kappaB target genes also requires phosphorylation of NF-kappaB proteins, such as p65, within their transactivation domain by a variety of kinases in response to distinct stimuli. Whether, and how, phosphorylation modulates the function of other NF-kappaB and IkappaB proteins, such as B-cell lymphoma 3, remains unclear. The identification and characterization of all the kinases known to phosphorylate NF-kappaB and IkappaB proteins are described here. Because deregulation of NF-kappaB and IkappaB phosphorylations is a hallmark of chronic inflammatory diseases and cancer, newly designed drugs targeting these constitutively activated signalling pathways represent promising therapeutic tools.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 09 April 2020
                Publication date Collection: April 2020
                Volume: 21
                Issue: 7
                Electronic Location Identifier: 2605
                Affiliations
                [1 ]Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy; silvia.zappavigna@ 123456unicampania.it (S.Z.); alessiamaria.cossu@ 123456biogem.it (A.M.C.); grim.anna@ 123456tiscali.it (A.G.); marco.bocchetti92@ 123456gmail.com (M.B.); michele.caraglia@ 123456unicampania.it (M.C.)
                [2 ]Biogem Scarl, Institute of Genetic Research, Laboratory of Molecular and Precision Oncology, 83031 Ariano Irpino, Italy
                [3 ]Multidisciplinary Department of Medical and Dental Specialties, University of Campania, “Luigi Vanvitelli”, Plastic Surgery Unit, 80138 Naples, Italy; giuseppe.ferraro@ 123456unicampania.it (G.A.F.); Giovannif.nicoletti@ 123456unicampania.it (G.F.N.)
                [4 ]Department of Science and Technology, University of Sannio, 82100 Benevento, Italy
                [5 ]Consorzio Sannio Tech-AMP Biotec, 82030 Apollosa, Italy
                Author notes
                Author information
                https://orcid.org/0000-0003-4787-3776
                https://orcid.org/0000-0002-2143-6669
                https://orcid.org/0000-0003-2408-6091
                Article
                Publisher ID: ijms-21-02605
                DOI: 10.3390/ijms21072605
                PMC ID: 7177823
                PubMed ID: 32283655
                SO-VID: 639e7c07-e502-4856-8a28-6643169c0d78
                Copyright © © 2020 by the authors.
                License:

                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
                Date received : 18 March 2020
                Date accepted : 07 April 2020
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: cancer,cox-2 inhibitors,embelin,inflammation-associated cancer,5-lox inhibitors,nsaids
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: cancer, cox-2 inhibitors, embelin, inflammation-associated cancer, 5-lox inhibitors, nsaids

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