ER stress-mediated autophagy promotes Myc-dependent transformation and tumor growth

The proto-oncogene c-Myc paradoxically activates both proliferation and apoptosis. In the pathogenic state, c-Myc-induced apoptosis is bypassed via a critical, yet poorly understood escape mechanism that promotes cellular transformation and tumorigenesis. The accumulation of unfolded proteins in the...

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Veröffentlicht in:	The Journal of clinical investigation 2012-12, Vol.122 (12), p.4621-4634
Hauptverfasser:	Hart, Lori S, Cunningham, John T, Datta, Tatini, Dey, Souvik, Tameire, Feven, Lehman, Stacey L, Qiu, Bo, Zhang, Haiyan, Cerniglia, George, Bi, Meixia, Li, Yan, Gao, Yan, Liu, Huayi, Li, Changhong, Maity, Amit, Thomas-Tikhonenko, Andrei, Perl, Alexander E, Koong, Albert, Fuchs, Serge Y, Diehl, J Alan, Mills, Ian G, Ruggero, Davide, Koumenis, Constantinos
Format:	Artikel
Sprache:	eng
Schlagworte:	Animal models Animals Apoptosis Autophagy Autophagy (Cytology) Biomedical research Biosynthesis Burkitt Lymphoma - metabolism Burkitt Lymphoma - pathology c-Myc protein Calcium Signaling Cancer Caspases - metabolism Cell cycle Cell Line, Tumor Cell Proliferation Cell Survival Cell Transformation, Neoplastic - metabolism Cluster Analysis Colonies eIF-2 Kinase - genetics eIF-2 Kinase - metabolism Endoplasmic reticulum Endoplasmic Reticulum Stress Enhancers Gene amplification Gene Knockout Techniques Genetic aspects Heterozygote Humans Hypoxia Initiation factor eIF-2 Kinases Lymphoma Malignancy Mice Oligonucleotide Array Sequence Analysis Phagocytosis Promoters (Genetics) Properties Protein biosynthesis Protein folding Protein synthesis Proteins Proto-Oncogene Proteins c-myc - metabolism Proto-Oncogene Proteins c-myc - physiology Proto-oncogenes Ribonucleic acid Ribosomal Proteins - genetics Ribosomal Proteins - metabolism RNA RNA polymerase Stress Transcription factors Transcriptome Transformation Tumorigenesis Unfolded Protein Response
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