ArticleThe Journal of biological chemistry2014
The translation initiation factor eIF3i up-regulates vascular endothelial growth factor A, accelerates cell proliferation, and promotes angiogenesis in embryonic development and tumorigenesis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- eIF3i facilitates NELFCD translation to promote metastasis via regulating EMT and invadopodia.British journal of cancer · 2026Article
- CAAP1 suppresses tumor growth and metastasis via interacting with EIF3I in high-grade serous ovarian carcinoma.American journal of cancer research · 2026Article
- mFrontiers in cell and developmental biology · 2026Review
- Trim28 citrullination maintains mouse embryonic stem cell pluripotency via regulating Nanog and Klf4 transcription.Science China. Life sciences · 2023Article
- Review
- Histone Deacetylase 1 Expression and Regulatory Network in Lung Adenocarcinoma Based on Data Mining and Implications for Targeted Treatment.Journal of oncology · 2023Article
- Molecular and Structural Characterization of Lenalidomide-Mediated Sequestration of eIF3i.ACS chemical biology · 2022Article
- Liver cancer cells with nuclear MET overexpression release translation regulatory protein-enriched extracellular vesicles exhibit metastasis promoting activity.Journal of extracellular biology · 2022Article
- Zebrafish Xenotransplantation Models for Studying Gene Function and Drug Treatment in Hepatocellular Carcinoma.Journal of gastrointestinal cancer · 2021Review
- Article
- Identification and Characterization of a Novel Protein ASP-3 Purified fromMarine drugs · 2019Article
- Article
- Systematically profiling the expression of eIF3 subunits in glioma reveals the expression of eIF3i has prognostic value in IDH-mutant lower grade glioma.Cancer cell international · 2019Article
- Mesoporous silicate nanoparticles/3D nanofibrous scaffold-mediated dual-drug delivery for bone tissue engineering.Journal of controlled release : official journal of the Controlled Release Society · 2018Article
- Lung epithelial-specific TRIP-1 overexpression maintains epithelial integrity during hyperoxia exposure.Physiological reports · 2018Article
- TRIP-1 Promotes the Assembly of an ECM That Contains Extracellular Vesicles and Factors That Modulate Angiogenesis.Frontiers in physiology · 2018Article
- eIF3i activity is critical for endothelial cells in tumor induced angiogenesis through regulating VEGFR and ERK translation.Oncotarget · 2017Article
- Human eIF3b and eIF3a serve as the nucleation core for the assembly of eIF3 into two interconnected modules: the yeast-like core and the octamer.Nucleic acids research · 2016Article
- TGF beta receptor II interacting protein-1, an intracellular protein has an extracellular role as a modulator of matrix mineralization.Scientific reports · 2016Article
- Clusterin facilitates metastasis by EIF3I/Akt/MMP13 signaling in hepatocellular carcinoma.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Vascular endothelial growth factor A (VEGFA) is a critical proangiogenic factor that is activated by hypoxia at both the transcriptional and post-transcriptional levels. In hypoxia conditions, stabilized hypoxia-inducible factor 1α (HIF1A) is the key regulator for transcriptional activation of VEGFA. However, the post-transcriptional control of VEGFA expression remains poorly understood. Here, we report that the eukaryotic translation initiation factor 3i (eIF3i) is required for VEGFA protein expression in both normal embryonic and tumorigenic angiogenesis. eIF3i is dynamically expressed in the early stages of zebrafish embryogenesis and in human hepatocellular carcinoma tissues. eIF3i homozygous mutant zebrafish embryos show severe angiogenesis defects and human hepatocellular cancer cells with depletion of eIF3i to induce less angiogenesis in tumor models. Under hypoxia, the HIF1A protein can interact with its binding sequence in the eIF3i promoter and activate eIF3i transcription. The expression of VEGFA, which should rise in hypoxia, is significantly inhibited by eIF3i siRNA treatment. Moreover, eIF3i knockdown did not cause a general translation repression but specifically reduced the translation efficiency of the VEGFA mRNAs. Taken together, our results suggest that eIF3i is induced by HIF1A under hypoxia and controls normal and tumorigenic angiogenesis through regulating VEGFA protein translation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.