ArticleOncogene2009
Regulation of non-AU-rich element containing c-fms proto-oncogene expression by HuR in breast cancer.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Human antigen R knockdown attenuates the invasive activity of oral cancer cells through inactivation of matrix metalloproteinase-1 gene expression.Journal of dental sciences · 2024Article
- RNA binding proteins (RBPs) and their role in DNA damage and radiation response in cancer.Advanced drug delivery reviews · 2022Review
- Hu Antigen R (HuR) Protein Structure, Function and Regulation in Hepatobiliary Tumors.Cancers · 2022Review
- Research progress on RNA-binding proteins in breast cancer.Oncology letters · 2022Review
- Roles of Embryonic Lethal Abnormal Vision-Like RNA Binding Proteins in Cancer and Beyond.Frontiers in cell and developmental biology · 2022Review
- Multifaceted roles of CCL20 (C-C motif chemokine ligand 20): mechanisms and communication networks in breast cancer progression.Bioengineered · 2021Review
- Regulation of closely juxtaposed proto-oncogeneRNA (New York, N.Y.) · 2021Article
- Phenotype of vigilin expressing breast cancer cells binding to the 69 nt 3'UTR element in CSF-1R mRNA.Translational oncology · 2019Article
- Suramin, screened from an approved drug library, inhibits HuR functions and attenuates malignant phenotype of oral cancer cells.Cancer medicine · 2018Article
- Clinical Significance and Biological Role of HuR in Head and Neck Carcinomas.Disease markers · 2018Review
- Human antigen R-regulated CCL20 contributes to osteolytic breast cancer bone metastasis.Scientific reports · 2017Article
- Musashi RNA-binding protein 2 regulates estrogen receptor 1 function in breast cancer.Oncogene · 2017Article
- Current Evidence and Future Perspectives on HuR and Breast Cancer Development, Prognosis, and Treatment.Neoplasia (New York, N.Y.) · 2016Review
- Autocrine inhibition of the c-fms proto-oncogene reduces breast cancer bone metastasis assessed with in vivo dual-modality imaging.Experimental biology and medicine (Maywood, N.J.) · 2014Article
- AngiotensinII induces HuR shuttling by post-transcriptional regulated CyclinD1 in human mesangial cells.Molecular biology reports · 2014Article
- Potent synergistic effect of IL-3 and TNF on matrix metalloproteinase 9 generation by human eosinophils.Cytokine · 2012Article
- The RNA-binding protein QKI5 is a direct target of C/EBPα and delays macrophage differentiation.Molecular biology of the cell · 2012Article
- HuR function in disease.Frontiers in bioscience (Landmark edition) · 2012Review
- Role of RNA binding protein HuR in ductal carcinoma in situ of the breast.The Journal of pathology · 2011Article
- Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer.Molecular and cellular biology · 2011Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of RNA-binding proteins in cancer biology is recognized increasingly. The nucleocytoplasmic shuttling and AU-rich RNA-binding protein HuR stabilizes several cancer-related target mRNAs. The proto-oncogene c-fms, whose 3'untranslated region (3'UTR) is not AU-rich, is associated with poor prognosis in breast cancer. Using a large breast-cancer tissue array (N=670), we found nuclear HuR expression to be associated with nodal metastasis and independently with poor survival (P=0.03, RR 1.45), as well as to be co-expressed with c-fms in the breast tumors (P=0.0007). We described c-fms mRNA as a direct target of HuR in vivo, and that HuR bound specifically to a 69-nt region containing 'CUU' motifs in 3'UTR c-fms RNA. Overexpressing or silencing HuR significantly up- or down-regulated c-fms RNA expression, respectively. We also found that known glucocorticoid stimulation of c-fms RNA and protein is largely dependent on the presence of HuR. HuR, by binding to the 69-nt wild type, but not mutant, c-fms sequence can regulate reporter gene expression post-transcriptionally. We are the first to describe that HuR can regulate gene expression by binding non-AU-rich sequences in 3'UTR c-fms RNA. Collectively, our findings suggest that HuR plays a supportive role for c-fms in breast cancer progression by binding a 69-nt element in its 3'UTR, thus regulating its expression.
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