TAILIEUCHUNG - Báo cáo khoa học: Apoptosis and autophagy: BIM as a mediator of tumour cell death in response to oncogene-targeted therapeutics

The BCL-2 homology domain 3 (BH3)-only protein, B-cell lymphoma 2 interacting mediator of cell death (BIM) is a potent pro-apoptotic protein belonging to the B-cell lymphoma 2 protein family. In recent years, advances in basic biology have provided a clearer picture of how BIM kills cells and how BIM expression and activity are repressed by growth factor signalling pathways, especially the extracellular signal-regulated kinase 1⁄2 and protein kinase B pathways. | MINIREVIEW Apoptosis and autophagy BIM as a mediator of tumour cell death in response to oncogene-targeted therapeutics Annette S. Gillings Kathryn Balmanno Ceri M. Wiggins Mark Johnson and Simon J. Cook Laboratory of Molecular Signalling The Babraham Institute Babraham Research Campus Cambridge UK Keywords B-celllymphoma 2 BCL-2 breakpoint cluster region Abelson murine leukaemia viraloncogene BCR ABL BCL-2-interacting mediator of cell death BIM v-raf murine sarcoma viral oncogene homologue B1 BRAF epidermalgrowth factor receptor EGFR extracellular signal-regulated kinase 1 2 ERK1 2 mitogen-mApK or ERK Kinase 1 2 MEK1 2 protein kinase B PKB ribosomalprotein S6 kinase RSK Correspondence Simon J. Cook Laboratory of Molecular Signalling The Babraham Institute Babraham Research Campus Cambridge CB22 3AT UK Fax 44-1223-496023 Tel 44-1223-496453 E-mail Received 16 March 2009 revised 23 June 2009 accepted 9 July 2009 The BCL-2 homology domain 3 BH3 -only protein B-cell lymphoma 2 interacting mediator of cell death BIM is a potent pro-apoptotic protein belonging to the B-cell lymphoma 2 protein family. In recent years advances in basic biology have provided a clearer picture of how BIM kills cells and how BIM expression and activity are repressed by growth factor signalling pathways especially the extracellular signal-regulated kinase 1 2 and protein kinase B pathways. In tumour cells these oncogene-regulated pathways are used to counter the effects of BIM thereby promoting tumour cell survival. In parallel a new generation of targeted therapeutics has been developed which show remarkable specificity and efficacy in tumour cells that are addicted to particular oncogenes. It is now apparent that the expression and activation of BIM is a common response to these new therapeutics. Indeed BIM has emerged from this marriage of basic and applied biology as an important mediator of tumour cell death in response to such drugs. The induction of BIM alone may

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