2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Melittin—A Natural Peptide from Bee Venom Which Induces Apoptosis in Human Leukaemia Cells

      research-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

          Bee venom is a very complex mixture produced and secreted by the honeybee ( Apis mellifera). Melittin is a major component of bee venom that accounts for about 52% of its dry mass. A vast number of studies have been dedicated to the effects of melittin’s regulation of apoptosis and to the factors that induce apoptosis in various types of cancer such as breast, ovarian, prostate, lung. The latest evidence indicates its potential as a therapeutic agent in the treatment of leukaemia. The aim of our present study is to evaluate melittin’s ability to induce apoptosis in leukaemia cell lines of different origin acute lymphoblastic leukaemia (CCRF-CEM) and chronic myelogenous leukaemia (K-562). We demonstrated that melittin strongly reduced cell viability in both leukaemia cell lines but not in physiological peripheral blood mononuclear cells (PMBCs). Subsequent estimated parameters (mitochondrial membrane potential, Annexin V binding and Caspases 3/7 activity) clearly demonstrated that melittin induced apoptosis in leukaemia cells. This is a very important step for research into the development of new potential anti-leukaemia as well as anticancer therapies. Further analyses on the molecular level have been also planned (analysis of proapoptotic genes expression and DNA damages) for our next research project, which will also focus on melittin.

          Related collections

          Most cited references48

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

          Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

          Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Acute lymphoblastic leukemia: a comprehensive review and 2017 update

            Acute lymphoblastic leukemia (ALL) is the second most common acute leukemia in adults, with an incidence of over 6500 cases per year in the United States alone. The hallmark of ALL is chromosomal abnormalities and genetic alterations involved in differentiation and proliferation of lymphoid precursor cells. In adults, 75% of cases develop from precursors of the B-cell lineage, with the remainder of cases consisting of malignant T-cell precursors. Traditionally, risk stratification has been based on clinical factors such age, white blood cell count and response to chemotherapy; however, the identification of recurrent genetic alterations has helped refine individual prognosis and guide management. Despite advances in management, the backbone of therapy remains multi-agent chemotherapy with vincristine, corticosteroids and an anthracycline with allogeneic stem cell transplantation for eligible candidates. Elderly patients are often unable to tolerate such regimens and carry a particularly poor prognosis. Here, we review the major recent advances in the treatment of ALL.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Melittin: a membrane-active peptide with diverse functions.

              Melittin is the principal toxic component in the venom of the European honey bee Apis mellifera and is a cationic, hemolytic peptide. It is a small linear peptide composed of 26 amino acid residues in which the amino-terminal region is predominantly hydrophobic whereas the carboxy-terminal region is hydrophilic due to the presence of a stretch of positively charged amino acids. This amphiphilic property of melittin has resulted in melittin being used as a suitable model peptide for monitoring lipid-protein interactions in membranes. In this review, the solution and membrane properties of melittin are highlighted, with an emphasis on melittin-membrane interaction using biophysical approaches. The recent applications of melittin in various cellular processes are discussed.
                Bookmark

                Author and article information

                Journal
                Biomolecules
                Biomolecules
                biomolecules
                Biomolecules
                MDPI
                2218-273X
                06 February 2020
                February 2020
                : 10
                : 2
                : 247
                Affiliations
                [1 ]Military Institute of Armament Technology, Prymasa Stefana Wyszyńskiego 7, 05-220 Zielonka, Poland; ceremugam@ 123456witu.mil.pl
                [2 ]CBRN Reconnaissance and Decontamination Department, Military Institute of Chemistry and Radiometry, Antoniego Chrusciela “Montera” 105, 00-910 Warsaw, Poland; m.stela@ 123456wichir.waw.pl
                [3 ]Biohazard Prevention Centre, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland; edyta.janik@ 123456unilodz.eu (E.J.); lmgorniak@ 123456gmail.com (L.G.)
                [4 ]Laboratory of Medical Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland; ewelina.synowiec@ 123456biol.uni.lodz.pl (E.S.); tomasz.sliwinski@ 123456biol.uni.lodz.pl (T.S.)
                [5 ]Department of Biology and Pharmaceutical Botany, Medical University of Lodz, 90-151 Lodz, Poland; przemyslaw.sitarek@ 123456umed.lodz.pl
                [6 ]Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland; joanna.saluk@ 123456biol.uni.lodz.pl
                Author notes
                [* ]Correspondence: michal.bijak@ 123456biol.uni.lodz.pl ; Tel./Fax: +48-42-635-43-36
                Author information
                https://orcid.org/0000-0001-8385-7744
                https://orcid.org/0000-0002-7838-4097
                Article
                biomolecules-10-00247
                10.3390/biom10020247
                7072249
                32041197
                71286909-5fc8-4a2d-8b80-f9372f4774a7
                © 2020 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
                : 27 December 2019
                : 04 February 2020
                Categories
                Article

                melittin,bee venom,apoptosis,leukaemia
                melittin, bee venom, apoptosis, leukaemia

                Comments

                Comment on this article