ArticleThe Journal of biological chemistry2013
RNPC1, an RNA-binding protein and a p53 target, regulates macrophage inhibitory cytokine-1 (MIC-1) expression through mRNA stability.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Emerging horizons on molecular and circulating biomarkers in pancreatic adenocarcinoma.Frontiers in oncology · 2024Review
- Fine-tuning p53 activity by modulating the interaction between eukaryotic translation initiation factor eIF4E and RNA-binding protein RBM38.Genes & development · 2021Article
- RBM38 in cancer: role and mechanism.Cellular and molecular life sciences : CMLS · 2021Review
- GDF15: A Hormone Conveying Somatic Distress to the Brain.Endocrine reviews · 2020Review
- RNA-Binding Motif Protein 38 as a Potential Biomarker and Therapeutic Target in Cancer.OncoTargets and therapy · 2020Review
- Cancer the'RBP'eutics-RNA-binding proteins as therapeutic targets for cancer.Pharmacology & therapeutics · 2019Review
- Disruption of the Rbm38-eIF4E Complex with a Synthetic Peptide Pep8 Increases p53 Expression.Cancer research · 2019Article
- Translating the Hypoxic Response-the Role of HIF Protein Translation in the Cellular Response to Low Oxygen.Cells · 2019Review
- RBM38 is involved in TGF-β-induced epithelial-to-mesenchymal transition by stabilising zonula occludens-1 mRNA in breast cancer.British journal of cancer · 2017Article
- The role of c-Myc-RBM38 loop in the growth suppression in breast cancer.Journal of experimental & clinical cancer research : CR · 2017Article
- PPM1D phosphatase, a target of p53 and RBM38 RNA-binding protein, inhibits p53 mRNA translation via dephosphorylation of RBM38.Oncogene · 2015Article
- Estrogen receptor (ER) was regulated by RNPC1 stabilizing mRNA in ER positive breast cancer.Oncotarget · 2015Article
- Hypoxia-inducible factor 1 alpha is regulated by RBM38, a RNA-binding protein and a p53 family target, via mRNA translation.Oncotarget · 2015Article
- Mice deficient in Rbm38, a target of the p53 family, are susceptible to accelerated aging and spontaneous tumors.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Implications of biomarkers in human hepatocellular carcinoma pathogenesis and therapy.World journal of gastroenterology · 2014Review
- Vasohibin‑2 promotes proliferation in human breast cancer cells via upregulation of fibroblast growth factor‑2 and growth/differentiation factor‑15 expression.Molecular medicine reports · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Macrophage inhibitory cytokine-1 (MIC-1), a secreted cytokine, is a direct target of p53 and known to play a role in cell proliferation, apoptosis, cell metastasis, and angiogenesis through autocrine and paracrine signaling. Previous studies have shown that serum levels of MIC-1 closely parallel cancer progression and are being explored as a diagnostic tool. MIC-1 has also shown potential as a therapeutic agent as it has exhibited several anti-carcinogenic activities. Thus, MIC-1 displays two opposing effects: tumor suppression versus promotion. However, it remains unclear whether MIC-1 is regulated by a mechanism other than transcription and how MIC-1 exerts its tumor suppression. In this study, we show that overexpression of RNA-binding protein RNPC1 can increase, whereas knockdown or knock-out of RNPC1 decreases, MIC-1 transcript and protein levels. Additionally, we demonstrate that RNPC1 can bind to MIC-1 mRNA via an AU-rich element within MIC-1 3'-UTR and then enhances MIC-1 mRNA stability. Finally, to explore the functional significance of MIC-1, we showed that knockdown of MIC-1 can decrease RNPC1-induced cell growth suppression. Altogether, we uncover a novel mechanism by which MIC-1 can be regulated through RNPC1 via mRNA stability.
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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.