ArticleOncotarget2016
IGF2-derived miR-483 mediated oncofunction by suppressing DLC-1 and associated with colorectal cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 35 citations in OpenAlex.
- 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
- Multi-modal clustering reveals event-free patient subgroup in colorectal cancer survival.NPJ systems biology and applications · 2025Article
- Identification and evaluation of a serum microRNA panel to diagnose colorectal cancer patients.International journal of cancer · 2025Article
- Article
- Synergic Action of Insulin-like Growth Factor-2 and miRNA-483 in Pterygium Pathogenesis.International journal of molecular sciences · 2023Article
- Treadmill training improves cognitive function by increasing IGF2 targeted downregulation of miRNA-483.Ibrain · 2022Article
- MiR-483 Promotes Colorectal Cancer Cell Biological Progression by Directly Targeting NDRG2 through Regulation of the PI3K/AKT Signaling Pathway and Epithelial-to-Mesenchymal Transition.Journal of healthcare engineering · 2022Article
- CBFβ promotes colorectal cancer progression through transcriptionally activating OPN, FAM129A, and UPP1 in a RUNX2-dependent manner.Cell death and differentiation · 2021Article
- ZBED6 regulates Igf2 expression partially through its regulation of miR483 expression.Scientific reports · 2021Article
- miRNA-mRNA Regulatory Network Reveals miRNAs in HCT116 in Response to Folic Acid Deficiency via Regulating Vital Genes of Endoplasmic Reticulum Stress Pathway.BioMed research international · 2021Article
- GH and IGF System: The Regulatory Role of miRNAs and lncRNAs in Cancer.Frontiers in endocrinology · 2021Review
- A Distinctive microRNA (miRNA) Signature in the Blood of Colorectal Cancer (CRC) Patients at Surgery.Cancers · 2020Article
- MicroRNA Regulation of the Small Rho GTPase Regulators-Complexities and Opportunities in Targeting Cancer Metastasis.Cancers · 2020Review
- Insulin-Like Growth Factor 2 (IGF2) Signaling in Colorectal Cancer-From Basic Research to Potential Clinical Applications.International journal of molecular sciences · 2019Review
- Mir-483 inhibits colon cancer cell proliferation and migration by targeting TRAF1.The Kaohsiung journal of medical sciences · 2018Article
- The Glucose-RegulatedCancers · 2018Review
- Role of miR-483 in digestive tract cancers: from basic research to clinical value.Journal of Cancer · 2018Review
- Infantile hemangioma: factors causing recurrence after propranolol treatment.Pediatric research · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence indicates that IGF2 plays an important role in various human malignancies, including colorectal cancer (CRC). Hsa-miR-483 is located within intron 7 of the IGF2 locus. However, the mechanism by which increased IGF2 induces carcinogenesis remains largely elusive. DLC-1 has been identified as a candidate tumor suppressor. In this study, we aimed at investigating whether miR-483 transcription is IGF2-dependent, identifying the functional target of miR-483, and evaluating whether tissue and serum miR-483-3p or miR-483-5p levels are associated with CRC. Our results showed that sequences upstream miR-483 had undetectable promoter activity and levels of IGF2, miR-483-3p, and miR-483-5p were synchronously increased in CRC tissues. Positive correlations between IGF2 and miR-483-3p (r=0.4984, ***p<0.0001), and between IGF2 and miR-483-5p (r=0.6659, ***p<0.0001) expression were found. In addition, patients with CRC had a significantly higher serum miR-483-5p level (*p<0.05) compared to normal controls. DLC-1 expression was decreased in colorectal cancer tissues and diminished through transient transfection with miR-483-3p. Our results suggest that IGF2 may exert its oncofunction, at least partly, through its parasitic miR-483 which suppressed DLC-1 in CRC cells. Thus, miR-483 might serve as a new target for therapy and a potential biomarker for the detection of colorectal cancer.
Indexed as
Identifiers
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.