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      Apoptosis, autophagy, necroptosis, and cancer metastasis

      research-article
      , , , ,
      Molecular Cancer
      BioMed Central
      Apoptosis, Autophagy, Necroptosis, Metastasis

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          Abstract

          Metastasis is a crucial hallmark of cancer progression, which involves numerous factors including the degradation of the extracellular matrix (ECM), the epithelial-to-mesenchymal transition (EMT), tumor angiogenesis, the development of an inflammatory tumor microenvironment, and defects in programmed cell death. Programmed cell death, such as apoptosis, autophagy, and necroptosis, plays crucial roles in metastatic processes. Malignant tumor cells must overcome these various forms of cell death to metastasize. This review summarizes the recent advances in the understanding of the mechanisms by which key regulators of apoptosis, autophagy, and necroptosis participate in cancer metastasis and discusses the crosstalk between apoptosis, autophagy, and necroptosis involved in the regulation of cancer metastasis.

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          Most cited references106

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          The role of Atg proteins in autophagosome formation.

          Macroautophagy is mediated by a unique organelle, the autophagosome, which encloses a portion of cytoplasm for delivery to the lysosome. Autophagosome formation is dynamically regulated by starvation and other stresses and involves complicated membrane reorganization. Since the discovery of yeast Atg-related proteins, autophagosome formation has been dissected at the molecular level. In this review we describe the molecular mechanism of autophagosome formation with particular focus on the function of Atg proteins and the long-standing discussion regarding the origin of the autophagosome membrane.
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            Live or let die: the cell's response to p53.

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              JNK signaling in apoptosis.

              Jun N-terminal kinases or JNKs play a critical role in death receptor-initiated extrinsic as well as mitochondrial intrinsic apoptotic pathways. JNKs activate apoptotic signaling by the upregulation of pro-apoptotic genes through the transactivation of specific transcription factors or by directly modulating the activities of mitochondrial pro- and antiapoptotic proteins through distinct phosphorylation events. This review analyses our present understanding of the role of JNK in apoptotic signaling and the various mechanisms by which JNK promotes apoptosis.
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                Author and article information

                Contributors
                suzhenyi999@163.com
                yangzuozhang@163.com
                xuyongqingkm@163.net
                ybchen@mail.kiz.ac.cn
                qyu@sibs.ac.cn
                Journal
                Mol Cancer
                Mol. Cancer
                Molecular Cancer
                BioMed Central (London )
                1476-4598
                21 February 2015
                21 February 2015
                2015
                : 14
                : 48
                Affiliations
                [ ]Department of Biochemistry and Molecular Biology, Medical School, Southeast University, Nanjing, Jiangsu 210009 China
                [ ]Department of Cell Biology, Harvard Medical School, Boston, MA 02115 USA
                [ ]Bone and Soft Tissue Tumors Research Center of Yunnan Province, Department of Orthopaedics, the Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 650118, China
                [ ]Department of Orthopaedics, Kunming General Hospital of Chengdu Military Command, Kunming, Yunnan 650118 China
                [ ]Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223 China
                [ ]Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai, 201203 China
                Article
                321
                10.1186/s12943-015-0321-5
                4343053
                25743109
                e4d1497f-df70-4149-a584-20859f3201e9
                © Su et al.; licensee BioMed Central. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 7 December 2014
                : 9 February 2015
                Categories
                Review
                Custom metadata
                © The Author(s) 2015

                Oncology & Radiotherapy
                apoptosis,autophagy,necroptosis,metastasis
                Oncology & Radiotherapy
                apoptosis, autophagy, necroptosis, metastasis

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