The DOI matches its Crossref record; 220 of the 227 references it cites were found in a registry or an index.
Targeting the eIF4F Translation Initiation Complex: A Critical Nexus for Cancer Development
Open accessAbstract
Elevated protein synthesis is an important feature of many cancer cells and often arises as a consequence of increased signaling flux channeled to eukaryotic initiation factor 4F (eIF4F), the key regulator of the mRNA–ribosome recruitment phase of translation initiation. In many cellular and preclinical models of cancer, eIF4F deregulation results in changes in translational efficiency of specific mRNA classes. Importantly, many of these mRNAs code for proteins that potently regulate critical cellular processes, such as cell growth and proliferation, enhanced cell survival and cell migration that ultimately impinge on several hallmarks of cancer, including increased angiogenesis, deregulated growth control, enhanced cellular survival, epithelial-to-mesenchymal transition, invasion, and metastasis. By being positioned as the molecular nexus downstream of key oncogenic signaling pathways (e.g., Ras, PI3K/AKT/TOR, and MYC), eIF4F serves as a direct link between important steps in cancer development and translation initiation. Identification of mRNAs particularly responsive to elevated eIF4F activity that typifies tumorigenesis underscores the critical role of eIF4F in cancer and raises the exciting possibility of developing new-in-class small molecules targeting translation initiation as antineoplastic agents. Cancer Res; 75(2); 250–63. ©2014 AACR.
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“Many direct eIF4A/eIF4F mRNA targets have been identified and often encode proteins that drive proliferation, metastasis, and survival (11, 14, 15).”
From Cotargeting a MYC/eIF4A-survival axis improves the efficacy of KRAS inhibitors in lung cancer (2023) · cites this paper as [11]
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2 retracted
Pardo, O. E., Arcaro, A., Salerno, G., Raguz, S., Downward, J., & Seckl, M. J. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.a115.109006 · Cited by 153
RetractedPardo, O. E., Arcaro, A., Salerno, G., Raguz, S., Downward, J., & Seckl, M. J. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m109006200 · Cited by 145
RetractedThe landscape of somatic copy-number alteration across human cancers
Beroukhim, R., Mermel, C. H., Porter, D., Wei, G., Raychaudhuri, S., Donovan, J., Barretina, J., Boehm, J. S., Dobson, J., Urashima, M., et al. (2010) · Nature · doi:10.1038/nature08822 · Cited by 4,017
Defining the role of mTOR in cancer
Guertin, D. A., & Sabatini, D. M. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.05.008 · Cited by 2,833
Molecular mechanisms of mTOR-mediated translational control
Ma, X. M., & Blenis, J. (2009) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2672 · Cited by 2,558
eIF4 Initiation Factors: Effectors of mRNA Recruitment to Ribosomes and Regulators of Translation
Gingras, A., Raught, B., & Sonenberg, N. (1999) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.68.1.913 · Cited by 2,103
Self-citationA unifying model for mTORC1-mediated regulation of mRNA translation
Thoreen, C. C., Chantranupong, L., Keys, H. R., Wang, T., Gray, N. S., & Sabatini, D. M. (2012) · Nature · doi:10.1038/nature11083 · Cited by 1,477
Regulation of 4E-BP1 phosphorylation: a novel two-step mechanismPreprint
Gingras, A., Gygi, S. P., Raught, B., Polakiewicz, R. D., Abraham, R. T., Hoekstra, M. F., Aebersold, R. H., & Sonenberg, N. (1999) · Genes & Development · doi:10.1101/gad.13.11.1422 · Cited by 1,348
Self-citationThe translational landscape of mTOR signalling steers cancer initiation and metastasis
Hsieh, A. C., Liu, Y., Edlind, M. P., Ingolia, N. T., Janes, M. R., Sher, A., Shi, E. Y., Stumpf, C. R., Christensen, C., Bonham, M. J., et al. (2012) · Nature · doi:10.1038/nature10912 · Cited by 1,313
Self-citationPhosphorylation and Functional Inactivation of TSC2 by Erk
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“Of the four phases of protein synthesis (initiation, elongation, termination, and recycling), initiation is considered to be the rate-limiting step in mRNA translation and is often exploited by cancer cells to support tumorigenesis (Pelletier et al., 2015).”
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Translation from unconventional 5′ start sites drives tumour initiation
Sendoel, A., Dunn, J. G., Rodriguez, E. H., Naik, S., Gomez, N. C., Hurwitz, B. S., Levorse, J. M., Dill, B. D., Schramek, D., Molina, H., et al. (2017) · Nature · doi:10.1038/nature21036 · Cited by 339
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Metadata
- Authors
- Pelletier, J., Graff, J., Ruggero, D., & Sonenberg, N.
- Affiliations
- Institut du cancer Rosalind & Morris Goodman (CA)
- Eli Lilly (United States) (US)
- University of California, San Francisco (US)
- Corresponding author
- Pelletier, Jerry
- Venue
- Cancer Research
- Published
- 2015-01-14
- Volume
- 75
- Issue
- 2
- Pages
- 250-263
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC4299928
- OpenAlex
- W2005176113
- Cited by
- 367
- References
- 227
- Citations by year
- 2026: 18 · 2025: 18 · 2024: 30 · 2023: 36 · 2022: 30 · 2021: 39 · 2020: 32 · 2019: 35 · 2018: 40 · 2017: 33 · 2016: 37 · 2015: 19
- FWCI
- 4.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship@McGill (McGill) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Public Health Service (MOP-106530, MOP-115126)
- National Cancer Institute (R01CA140456, R01CA184624, R01CA154916)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA modifications and cancer
- Keywords
- eIF4F, translation initiation, cancer, translational regulation, oncogenic signaling, Ras, c-Myc, metastasis, epithelial-mesenchymal transition, angiogenesis, cell proliferation
- MeSH terms
- Animals, Antineoplastic Agents, Humans, Neoplasms, Eukaryotic Initiation Factor-4F, Molecular Targeted Therapy
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