ArticleOncotarget2017
MiR-766 induces p53 accumulation and G2/M arrest by directly targeting MDM4.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed.
- Tumor Suppressor p53 and MicroRNAs Interaction in Breast Cancer.Oncology research · 2026Review
- A Critical Review on microRNAs as Prognostic Biomarkers in Laryngeal Carcinoma.International journal of molecular sciences · 2024Review
- Human mesenchymal stroma/stem-like cell-derived taxol-loaded EVs/exosomes transfer anti-tumor microRNA signatures and express enhanced SDF-1-mediated tumor tropism.Cell communication and signaling : CCS · 2024Article
- Non-coding RNAs as therapeutic targets in cancer and its clinical application.Journal of pharmaceutical analysis · 2024Review
- The crosstalk between non-coding RNAs and cell-cycle events: A new frontier in cancer therapy.Molecular therapy. Oncology · 2024Review
- The key role of microRNA-766 in the cancer development.Frontiers in oncology · 2023Review
- Plasma miR-151-3p as a Candidate Diagnostic Biomarker for Head and Neck Cancer: A Cross-sectional Study within the INHANCE Consortium.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022Article
- From inflammatory bowel disease to colorectal cancer: what's the role of miRNAs?Cancer cell international · 2022Review
- Non-coding RNA in cancer.Essays in biochemistry · 2021Review
- The roles and regulation of MDM2 and MDMX: it is not just about p53.Genes & development · 2021Review
- Article
- MDM4 alternative splicing and implication in MDM4 targeted cancer therapies.American journal of cancer research · 2021Review
- MicroRNA-766 Promotes The Proliferation, Migration And Invasion, And Inhibits The Apoptosis Of Cutaneous Squamous Cell Carcinoma Cells By Targeting PDCD5.OncoTargets and therapy · 2020Article
- CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer.Cell cycle (Georgetown, Tex.) · 2019Article
- miRNA-766 induces apoptosis of human colon cancer cells through the p53/Bax signaling pathway by MDM4.Experimental and therapeutic medicine · 2019Article
- Melatonin is a potential inhibitor of ovarian cancer: molecular aspects.Journal of ovarian research · 2019Review
- The long and the short of it: the MDM4 tail so far.Journal of molecular cell biology · 2019Review
- MicroRNA-766-3p Inhibits Tumour Progression by Targeting Wnt3a in Hepatocellular Carcinoma.Molecules and cells · 2018Article
- Oncogenic and Tumor-Suppressive Roles of MicroRNAs with Special Reference to Apoptosis: Molecular Mechanisms and Therapeutic Potential.Molecular diagnosis & therapy · 2018Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53, a transcription factor that participates in multiple cellular functions, is considered the most important tumor suppressor. Previous evidence suggests that post-transcriptional deregulation of p53 by microRNAs contributes to tumorigenesis, tumor progression and therapeutic resistance. In the present study, we found that the microRNA miR-766 was aberrantly expressed in breast cancer, and that over-expression of miR-766 caused accumulation of wild-type p53 protein in multiple cancer cell lines. Supporting its role in the p53 signalling pathway, miR-766 decreased cell proliferation and colony formation in several cancer cell lines, and cell cycle analyses revealed that miR-766 causes G2 arrest. At a mechanistic level, we demonstrate that miR-766 enhances p53 signalling by directly targeting MDM4, an oncogene and negative regulator of p53. Analysis of clinical genomic data from multiple cancer types supports the relevance of miR-766 in p53 signalling. Collectively, our study demonstrates that miR-766 can function as a novel tumor suppressor by enhancing p53 signalling.
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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.