ArticleCancer research2010
Oncogenic role of miR-483-3p at the IGF2/483 locus.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
125 citing papers in PubMed, 213 citations in OpenAlex.
- miR-483 Targeting of CTGF Suppresses Endothelial-to-Mesenchymal Transition: Therapeutic Implications in Kawasaki Disease.Circulation research · 2017Trial
- Integrated microRNA and mRNA responses to acute human left ventricular ischemia.Physiological genomics · 2015Trial
- Trial
- Global microRNA profiling in favorable prognosis subgroups of cancer of unknown primary (CUP) demonstrates no significant expression differences with metastases of matched known primary tumors.Clinical & experimental metastasis · 2013Trial
- MicroRNA expression signatures associated with metastatic progression in papillary thyroid carcinoma.Archives of endocrinology and metabolism · 2026Article
- Integrative Regulatory Networks of MicroRNA-483: Unveiling Its Systematic Role in Human Diseases and Clinical Implications.Biomolecules · 2025Review
- A microRNA CRISPR screen reveals microRNA-483-3p as an apoptotic regulator in prostate cancer cells.Cell death & disease · 2025Article
- Potential Utility of Circulating MicroRNA-483 as a Biomarker for IGF-II-Associated Non-Islet Cell Tumor Hypoglycemia.The Journal of clinical endocrinology and metabolism · 2025Article
- Hsa-MiR-483 -3p regulates the extracellular matrix proteins via TGFβ2/SMAD4 signaling in the glucocorticoid-responsive human trabecular meshwork cells.Cell and tissue research · 2025Article
- Evaluation of microRNAs as liquid biopsy markers in adrenocortical tumors.Frontiers in endocrinology · 2025Article
- Molecular and Genetics Perspectives on Primary Adrenocortical Hyperfunction Disorders.International journal of molecular sciences · 2024Review
- Circulating non-coding RNA biomarkers of endocrine tumours.Nature reviews. Endocrinology · 2024Review
- The Potential of Circulating miR-193b, miR-146b-3p and miR-483-3p as Noninvasive Biomarkers in Cutaneous Melanoma Patients.Molecular biotechnology · 2024Article
- Overexpression of Igf2-derived Mir483 inhibits Igf1 expression and leads to developmental growth restriction and metabolic dysfunction in mice.Cell reports · 2024Article
- CRISPR-Cas9 screens reveal common essential miRNAs in human cancer cell lines.Genome medicine · 2024Article
- Article
- Integrative Transcriptomic Profiling of the Wilms Tumor.Cancers · 2023Article
- MicroRNA 483-3p overexpression unleashes invasive growth of metastatic colorectal cancer via NDRG1 downregulation and ensuing activation of the ERBB3/AKT axis.Molecular oncology · 2023Article
- Human IGF2 Gene Epigenetic and Transcriptional Regulation: At the Core of Developmental Growth and Tumorigenic Behavior.Biomedicines · 2023Review
- Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
hsa-mir-483 is located within intron 2 of the IGF2 locus. We found that the mature microRNA (miRNA) miR-483-3p is overexpressed in 100% of Wilms' tumors. In addition, colon, breast, and liver cancers exhibit high or even extremely high levels of miR-483-3p in approximately 30% of the cases. A coregulation with IGF2 mRNA was detected, although some tumors exhibited high expression of miR-483-3p without a concomitant increase of IGF2. These findings suggested that miR-483-3p could cooperate with IGF2 or act as an autonomous oncogene. Indeed, here we prove that an anti-miRNA oligonucleotide against miR-483-3p could inhibit the miRNAs without affecting IGF2 mRNA and it could suppress tumorigenicity of HepG2 cells, a cell line that overexpresses miR-483-3p and IGF2. Conversely, no antitumor effect was elicited by inhibition of IGF2. The oncogenic mechanism of miR-483-3p was at least partially clarified by the finding that it could modulate the proapoptotic protein BBC3/PUMA and miR-483-3p enforced expression could protect cells from apoptosis. Our results indicate that miR-483-3p could function as an antiapoptotic oncogene in various human cancers and reveal a new, potentially important target for anticancer therapy.
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What OpenQuestion holds
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.