The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Differential Requirements for eIF4E Dose in Normal Development and Cancer
Open accessAbstract
SUMMARY eIF4E, the major cap-binding protein, has long been considered limiting for translating the mammalian genome. However, the requirement for eIF4E dose at an organismal level remains unexplored. By generating an Eif4e haploinsufficient mouse, we found that 50% reduction in eIF4E expression, while compatible with normal development and global protein synthesis, significantly impeded cellular transformation. Genome-wide translational profiling uncovered a translational program induced by oncogenic transformation and revealed a critical role for eIF4E dose specifically in translating a network of mRNAs enriched for a unique 5′UTR signature. In particular, we demonstrate that eIF4E dose is essential for translating mRNAs regulating reactive oxygen species that fuel transformation and cancer cell survival in vivo. Our findings indicate that cancer cells hijack the eIF4E level in excess for normal development to drive a translational program supporting tumorigenesis.
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1 retracted
Selective killing of cancer cells by a small molecule targeting the stress response to ROS
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RNA-Binding Proteins in Cancer: Old Players and New Actors
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Self-citationNew frontiers in translational control of the cancer genome
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Self-citationRNA-binding proteins in tumor progression
Qin, H., Ni, H., Liu, Y., Yuan, Y., Xi, T., Li, X., & Zheng, L. (2020) · Journal of Hematology & Oncology · doi:10.1186/s13045-020-00927-w · Cited by 375
Oncogenic Roles of the PI3K/AKT/mTOR axis
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Metadata
- Authors
- Truitt, M. L., Conn, C. S., Shi, Z., Pang, X., Tokuyasu, T., Coady, A. M., Seo, Y., Barna, M., & Ruggero, D.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 162
- Issue
- 1
- Pages
- 59-71
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W1608233475
- Cited by
- 368
- References
- 45
- FWCI
- 11.96
- Type
- journal article
- Language
- en
- Open access
- bronze
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