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      Bcl-2 Inhibition to Overcome Resistance to Chemo- and Immunotherapy

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          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

          According to the World Health Organization (WHO), cancer is a leading cause of death worldwide. The identification of novel targets for cancer treatment is an area of intense work that has led Bcl-2 over-expression to be proposed as one of the hallmarks of cancer and Bcl-2 inhibition as a promising strategy for cancer treatment. In this review, we describe the different pathways related to programmed cell death, the role of Bcl-2 family members in apoptosis resistance to anti-cancer treatments, and the potential utility of Bcl-2 inhibitors to overcome resistance to chemo- and immunotherapy.

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          Programmed cell death pathways in cancer: a review of apoptosis, autophagy and programmed necrosis.

          L Ouyang, Z. Shi, S. Zhao … (2012)
          Programmed cell death (PCD), referring to apoptosis, autophagy and programmed necrosis, is proposed to be death of a cell in any pathological format, when mediated by an intracellular program. These three forms of PCD may jointly decide the fate of cells of malignant neoplasms; apoptosis and programmed necrosis invariably contribute to cell death, whereas autophagy can play either pro-survival or pro-death roles. Recent bulk of accumulating evidence has contributed to a wealth of knowledge facilitating better understanding of cancer initiation and progression with the three distinctive types of cell death. To be able to decipher PCD signalling pathways may aid development of new targeted anti-cancer therapeutic strategies. Thus in this review, we present a brief outline of apoptosis, autophagy and programmed necrosis pathways and apoptosis-related microRNA regulation, in cancer. Taken together, understanding PCD and the complex interplay between apoptosis, autophagy and programmed necrosis may ultimately allow scientists and clinicians to harness the three types of PCD for discovery of further novel drug targets, in the future cancer treatment. © 2012 Blackwell Publishing Ltd.
          Article 0 comments Cited 470 times – based on 0 reviews     Review now
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            Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis.

            Jerry E Chipuk, Tomomi Kuwana, Lisa Bouchier-Hayes … (2004)
            The tumor suppressor p53 exerts its anti-neoplastic activity primarily through the induction of apoptosis. We found that cytosolic localization of endogenous wild-type or trans-activation-deficient p53 was necessary and sufficient for apoptosis. p53 directly activated the proapoptotic Bcl-2 protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program. p53 also released both proapoptotic multidomain proteins and BH3-only proteins [Proapoptotic Bcl-2 family proteins that share only the third Bcl-2 homology domain (BH3)] that were sequestered by Bcl-xL. The transcription-independent activation of Bax by p53 occurred with similar kinetics and concentrations to those produced by activated Bid. We propose that when p53 accumulates in the cytosol, it can function analogously to the BH3-only subset of proapoptotic Bcl-2 proteins to activate Bax and trigger apoptosis.
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              Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis.

              E Oda, R Ohki, H Murasawa … (2000)
              A critical function of tumor suppressor p53 is the induction of apoptosis in cells exposed to noxious stresses. We report a previously unidentified pro-apoptotic gene, Noxa. Expression of Noxa induction in primary mouse cells exposed to x-ray irradiation was dependent on p53. Noxa encodes a Bcl-2 homology 3 (BH3)-only member of the Bcl-2 family of proteins; this member contains the BH3 region but not other BH domains. When ectopically expressed, Noxa underwent BH3 motif-dependent localization to mitochondria and interacted with anti-apoptotic Bcl-2 family members, resulting in the activation of caspase-9. We also demonstrate that blocking the endogenous Noxa induction results in the suppression of apoptosis. Noxa may thus represent a mediator of p53-dependent apoptosis.
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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): 08 December 2018
                Publication date Collection: December 2018
                Volume: 19
                Issue: 12
                Electronic Location Identifier: 3950
                Affiliations
                [1 ]Research Unit, REDISSEC, Hospital Costa del Sol, Autovía A-7, km 187, 29603 Marbella, Málaga, Spain; marilina@ 123456hcs.es
                [2 ]Oncology Department, Hospital Costa del Sol, Autovía A-7, km 187, 29603 Marbella, Málaga, Spain; eliperu@ 123456gmail.es
                [3 ]Research Unit, REDISSEC, Hospital Costa del Sol, Universidad de Málaga, Autovía A-7 km 187, 29603 Marbella, Málaga, Spain
                Author notes
                [* ]Correspondence: mredondo@ 123456hcs.es
                Article
                Publisher ID: ijms-19-03950
                DOI: 10.3390/ijms19123950
                PMC ID: 6321604
                PubMed ID: 30544835
                SO-VID: e658ab56-068b-4228-9b39-b89087814427
                Copyright © © 2018 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 : 29 October 2018
                Date accepted : 06 December 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: bcl-2,resistance,apoptosis,inhibition,cancer,chemotherapy,immunotherapy
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: bcl-2, resistance, apoptosis, inhibition, cancer, chemotherapy, immunotherapy

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