Journal
NATURE MEDICINE
Volume 18, Issue 1, Pages 83-90Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.2540
Keywords
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Funding
- Instituto de Salud Carlos-Fondos Europeos de Desarrollo Regional (FEDER) [PI080421]
- Ministerio de Ciencia e Innovacion (MICINN)
- Fundacio La MaratoTV3 [051110]
- American Institute for Cancer Research (AICR) [11-0086]
- Generalitat de Catalunya [2009SGR1409, 2009SGR1436]
- Consolider RNAREG from MICINN [CSD2009-00080]
- AICR [11-0086]
- Xarxa de Bancs de
- Pla Director d'Oncologia de Catalunya
- Instituto de Salud Carlos III
- Departament de Sanitat de la Generalitat de Catalunya
- MICINN
- Fundacion Ramon Areces
- DURSI (Generalitat de Catalunya)
- Eons Social Europeu (ESF)
- [BFU2008-02373]
- ICREA Funding Source: Custom
- Worldwide Cancer Research [11-0086] Funding Source: researchfish
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Malignant transformation, invasion and angiogenesis rely on the coordinated reprogramming of gene expression in the cells from which the tumor originated. Although deregulated gene expression has been extensively studied at genomic and epigenetic scales, the contribution of the regulation of mRNA-specific translation to this reprogramming is not well understood. Here we show that cytoplasmic polyadenylation element binding protein 4 (CPEB4), an RNA binding protein that mediates meiotic mRNA cytoplasmic polyadenylation and translation, is overexpressed in pancreatic ductal adenocarcinomas and glioblastomas, where it supports tumor growth, vascularization and invasion. We also show that, in pancreatic tumors, the pro-oncogenic functions of CPEB4 originate in the translational activation of mRNAs that are silenced in normal tissue, including the mRNA of tissue plasminogen activator, a key contributor to pancreatic ductal adenocarcinoma malignancy. Taken together, our results document a key role for post-transcriptional gene regulation in tumor development and describe a detailed mechanism for gene expression reprogramming underlying malignant tumor progression.
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