29
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Autophagy as a cell death and tumor suppressor mechanism.

      Oncogene

      Animals, Ubiquitin, Signal Transduction, physiology, Phosphatidylinositol 3-Kinases, Oncogenes, therapy, pathology, etiology, Neoplasms, metabolism, Lysosomes, Humans, Heat-Shock Proteins, HSP70 Heat-Shock Proteins, GTP-Binding Proteins, Eukaryotic Initiation Factor-2, Death-Associated Protein Kinases, Cell Transformation, Neoplastic, Calcium-Calmodulin-Dependent Protein Kinases, Autophagy, Apoptosis Regulatory Proteins, Apoptosis

      Read this article at

      ScienceOpenPublisherPubMed
      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

          Autophagy is characterized by sequestration of bulk cytoplasm and organelles in double or multimembrane autophagic vesicles, and their delivery to and subsequent degradation by the cell's own lysosomal system. Autophagy has multiple physiological functions in multicellular organisms, including protein degradation and organelle turnover. Genes and proteins that constitute the basic machinery of the autophagic process were first identified in the yeast system and some of their mammalian orthologues have been characterized as well. Increasing lines of evidence indicate that these molecular mechanisms may be recruited by an alternative, caspase-independent form of programmed cell death, named autophagic type II cell death. In some settings, autophagy and apoptosis seem to be interconnected positively or negatively, introducing the concept of 'molecular switches' between them. Additionally, mitochondria may be central organelles integrating the two types of cell death. Malignant transformation is frequently associated with suppression of autophagy. The recent implication of tumor suppressors like Beclin 1, DAP-kinase and PTEN in autophagic pathways indicates a causative role for autophagy deficiencies in cancer formation. Autophagic cell death induction by some anticancer agents underlines the potential utility of its induction as a new cancer treatment modality.

          Related collections

          Author and article information

          Journal
          15077152
          10.1038/sj.onc.1207521

          Comments

          Comment on this article