Impaired ribosome biogenesis checkpoint activation induces p53-dependent MCL-1 degradation and MYC-driven lymphoma death

MYC-driven B-cell lymphomas are addicted to increased levels of ribosome biogenesis (RiBi), offering the potential for therapeutic intervention. However, it is unclear whether inhibition of RiBi suppresses lymphomagenesis by decreasing translational capacity and/or by p53 activation mediated by the...

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Veröffentlicht in:	Blood 2021-06, Vol.137 (24), p.3351-3364
Hauptverfasser:	Domostegui, Ana, Peddigari, Suresh, Mercer, Carol A., Iannizzotto, Flavia, Rodriguez, Marta L., Garcia-Cajide, Marta, Amador, Virginia, Diepstraten, Sarah T., Kelly, Gemma L., Salazar, Ramón, Kozma, Sara C., Kusnadi, Eric P., Kang, Jian, Gentilella, Antonio, Pearson, Richard B., Thomas, George, Pelletier, Joffrey
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell Cycle Checkpoints - drug effects Cell Cycle Checkpoints - genetics Cell Line, Tumor Dactinomycin - pharmacology Lymphoid Neoplasia Lymphoma, B-Cell - drug therapy Lymphoma, B-Cell - genetics Lymphoma, B-Cell - metabolism Male Mice Myeloid Cell Leukemia Sequence 1 Protein - genetics Myeloid Cell Leukemia Sequence 1 Protein - metabolism Proteolysis - drug effects Proto-Oncogene Proteins c-myc - genetics Proto-Oncogene Proteins c-myc - metabolism Ribosomal Proteins - antagonists & inhibitors Ribosomal Proteins - genetics Ribosomal Proteins - metabolism Ribosomes - genetics Ribosomes - metabolism RNA, Neoplasm - genetics RNA, Neoplasm - metabolism RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism
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