ArticlePloS one2016
IRF1 Downregulation by Ras/MEK Is Independent of Translational Control of IRF1 mRNA.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- A new strategy for treating colorectal cancer: Regulating the influence of intestinal flora and oncolytic virus on interferon.Molecular therapy oncolytics · 2023Review
- Interferon regulatory factor 3 mediates effective antiviral responses to human coronavirus 229E and OC43 infection.Frontiers in immunology · 2023Article
- A Pyroptosis-Related Gene Signature Predicts Prognosis and Immune Microenvironment for Breast Cancer Based on Computational Biology Techniques.Frontiers in genetics · 2022Article
- Fibroblast Growth Factor 2 Enhances Zika Virus Infection in Human Fetal Brain.The Journal of infectious diseases · 2019Article
- IRF1 inhibits the proliferation and metastasis of colorectal cancer by suppressing the RAS-RAC1 pathway.Cancer management and research · 2019Article
- XAF1 forms a positive feedback loop with IRF-1 to drive apoptotic stress response and suppress tumorigenesis.Cell death & disease · 2018Article
- Mechanisms underlying the antiproliferative effects of a series of quinoxaline-derived chalcones.Scientific reports · 2017Article
- The MEK Inhibitors Trametinib and Cobimetinib Induce a Type I Interferon Response in Human Keratinocytes.International journal of molecular sciences · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenic activation of Ras/MEK downregulates the expression of interferon regulatory factor 1 (IRF1), which is a prerequisite for oncolytic viruses to replicate in cancer cells [1]. Moreover, restoration of IRF1 expression is essential to induce apoptosis of cancer cells treated with a MEK inhibitor [2]. However, the molecular mechanisms that underlie IRF1 downregulation by Ras/MEK remain unclear. In this study, we determined whether Ras/MEK activation modulates IRF1 expression at its translational level. MEK inhibition increased the activity of IRF1 promoter construct in Ras transformed NIH3T3 cells and wild type MEF, but not in IRF1 deficient MEF, indicating that IRF1 protein is required for the transcriptional activation of IRF1. By conducting reporter analysis using IRF1 5'- and 3'- UTR constructs, we determined that cis elements on 5'- and 3'-UTR of IRF1 mRNA are not involved in the IRF1 regulation by Ras/MEK. We further compared the recruitment of ribosomes to IRF1 mRNA in RasV12 cells treated with or without the MEK inhibitor by conducting polysome analysis. No difference was observed in the polysomal distribution of IRF1 mRNA between RasV12 cells treated with and without the MEK inhibitor. These results suggest that regulation of IRF1 translation is independent of IRF1 downregulation by Ras/MEK.
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