ArticleOncogene2019
miR-155 drives oncogenesis by promoting and cooperating with mutations in the c-Kit oncogene.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.
- The relationship of miR-155 host gene polymorphism in the susceptibility of cancer: a systematic review and meta-analysis.Frontiers in genetics · 2025Pooled it
- A Meta-Analysis of MiRNA-497 and Prognosis of Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2024Pooled it
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- Decoding the Promise and Challenges of miRNA-Based Cancer Therapies: An Essential Update on miR-21, miR-34, and miR-155.International journal of medical sciences · 2024Review
- Salivary level of microRNA-146a and microRNA-155 biomarkers in patients with oral lichen planus versus oral squamous cell carcinoma.BMC oral health · 2023Article
- miRNA: A Promising Therapeutic Target in Cancer.International journal of molecular sciences · 2022Review
- MicroRNA networks in FLT3-ITD acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Role of MiRNA in Cancer: Pathogenesis, Diagnosis, and Treatment.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Dysregulation of miRNAs in DLBCL: Causative Factor for Pathogenesis, Diagnosis and Prognosis.Diagnostics (Basel, Switzerland) · 2021Review
- RNA in cancer.Nature reviews. Cancer · 2021Review
- TERF1 downregulation promotes the migration and invasion of the PC3 prostate cancer cell line as a target of miR‑155.Molecular medicine reports · 2020Article
- Targeting AGTR1/NF-κB/CXCR4 axis by miR-155 attenuates oncogenesis in glioblastoma.Neoplasia (New York, N.Y.) · 2020Article
- Mouse bone marrow mesenchymal stem cells with distinct p53 statuses display differential characteristics.Molecular medicine reports · 2020Article
- MicroRNA-144 targets APP to regulate AML1/ETOOncology letters · 2019Article
- A Potential Tumor Suppressor Gene Named miR-508-5p Inhibited the Proliferation and Invasion of Human Melanoma Cells by Targeting KIT.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have emerged as crucial players in the development and maintenance of disease. miR-155 is an inflammation-associated, oncogenic miRNA, frequently overexpressed in hematological malignancies and solid tumors. However, the mechanism of oncogenesis by miR-155 is not well characterized, and research has focused primarily on individual, direct targets, which does not recapitulate the complexities of cancer. Using a powerful, inducible transgenic mouse model that overexpresses miR-155 and develops miR-155-addicted hematological malignancy, we describe here a multi-step process of oncogenesis by miR-155, which involves cooperation between miR-155, its direct targets, and other oncogenes. miR-155 is known to target DNA-repair proteins, leading to a mutator phenotype, and we find that over 93% of tumors in our miR-155 overexpressing mice contain activating mutations in a single oncogene, c-Kit. Treating mice with dasatinib or imatinib, which target c-Kit, resulted in complete tumor regression, indicating that c-Kit activity is crucial in the oncogenic process. Interestingly, c-Kit expression is high when miR-155 is overexpressed, indicating further cooperation between miR-155 and c-Kit. Our findings support a multi-step model of oncogenesis by miR-155 in which miR-155 promotes both a mutator phenotype and a cellular environment particularly susceptible to mutations in a given oncogene.
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.