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

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          Abstract

          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 micro RNA 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.

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          Author and article information

          Journal
          Cell Prolif
          Cell Prolif
          10.1111/(ISSN)1365-2184
          CPR
          Cell Proliferation
          John Wiley and Sons Inc. (Hoboken )
          0960-7722
          1365-2184
          03 October 2012
          December 2012
          : 45
          : 6 ( doiID: 10.1111/cpr.2012.45.issue-6 )
          : 487-498
          Affiliations
          [ 1 ] State Key Laboratory of Biotherapy and Cancer Center West China Hospital, Sichuan University Chengdu China
          [ 2 ] Key Laboratory of Bio‐resources and Eco‐environment, Ministry of Education, School of Life Sciences Sichuan University Chengdu China
          [ 3 ] School of Life Sciences Guizhou Normal University Guiyang China
          [ 4 ] Shanghai Key Laboratory for Pharmaceutical Metabolite Research, School of Pharmacy Second Military Medical University Shanghai China
          Author notes
          [* ]Correspondence: T.‐T. Zhou, Shanghai Key Laboratory for Pharmaceutical Metabolite Research, School of Pharmacy, Second Military Medical University, No. 325 Guohe Road, Shanghai 200433, China. Tel/Fax: +86‐28‐85415171; E‐mail: ting0618@ 123456tom.com ; B. Liu, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, China. E‐mail: liubo2400@ 123456163.com and J.‐K. Bao, Key Laboratory of Bio‐resources and Eco‐environment, Ministry of Education, School of Life Sciences, Sichuan University, Chengdu 610064, China. E‐mail: jinkubao@ 123456126.com
          [†]

          These authors contributed equally to this work.

          Article
          PMC6496669 PMC6496669 6496669 CPR845
          10.1111/j.1365-2184.2012.00845.x
          6496669
          23030059
          © 2012 Blackwell Publishing Ltd
          Page count
          Pages: 12
          Funding
          Funded by: Young Teacher's Fund of Sichuan University
          Award ID: 2010SCU11066
          Funded by: Science Foundation for Post Doctorate Research of China
          Award ID: 20110491725
          Funded by: Major State Basic Research Development Program of China (973 Program)
          Award ID: 2010cb529900
          Categories
          Review Article
          Review Articles
          Custom metadata
          2.0
          cpr845
          December 2012
          Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.2.1 mode:remove_FC converted:02.05.2019

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