ArticleOncotarget2016
microRNA-206 impairs c-Myc-driven cancer in a synthetic lethal manner by directly inhibiting MAP3K13.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Bioinformatic analysis and experimental validation of the function of mitogen-activated protein kinase in esophageal cancer.Discover oncology · 2026Article
- Evolving copy number gains promote tumor expansion and bolster mutational diversification.Nature communications · 2024Article
- Advances in synthetic lethality modalities for glioblastoma multiforme.Open medicine (Warsaw, Poland) · 2024Review
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- Article
- Clinical significance of mitogen-activated protein kinase kinase kinases in hepatitis B virus -related hepatocellular carcinoma and underlying mechanism exploration.Bioengineered · 2022Article
- Clinicopathological and Genomic Features of Pediatric Intracranial Myxoid Mesenchymal Tumor with both ofNMC case report journal · 2022Article
- LINC01287 facilitates proliferation, migration, invasion and EMT of colon cancer cells via miR-4500/MAP3K13 pathway.BMC cancer · 2021Article
- KMT2D promotes proliferation of gastric cancer cells: evidence from ctDNA sequencing.Journal of clinical laboratory analysis · 2021Article
- Wallenda-Nmo Axis Regulates Growth via Hippo Signaling.Frontiers in cell and developmental biology · 2021Article
- Inhibition of miR-1193 leads to synthetic lethality in glioblastoma multiforme cells deficient of DNA-PKcs.Cell death & disease · 2020Article
- The MAP3K13-TRIM25-FBXW7α axis affects c-Myc protein stability and tumor development.Cell death and differentiation · 2020Article
- Multitasking: Dual Leucine Zipper-Bearing Kinases in Neuronal Development and Stress Management.Annual review of cell and developmental biology · 2019Review
- MYC-related microRNAs signatures in non-Hodgkin B-cell lymphomas and their relationships with core cellular pathways.Oncotarget · 2018Article
- Pterostilbene down-regulates hTERT at physiological concentrations in breast cancer cells: Potentially through the inhibition of cMyc.Journal of cellular biochemistry · 2018Article
- MicroRNA-148a deficiency promotes hepatic lipid metabolism and hepatocarcinogenesis in mice.Cell death & disease · 2017Article
- MicroRNA-30a attenuates mutant KRAS-driven colorectal tumorigenesis via direct suppression of ME1.Cell death and differentiation · 2017Article
- Synthetic lethality: emerging targets and opportunities in melanoma.Pigment cell & melanoma research · 2017Review
- MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN.Oncotarget · 2017Article
- Strategies to Inhibit Myc and Their Clinical Applicability.Frontiers in cell and developmental biology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
c-Myc (Myc) is one of the most frequently dysregulated oncogenic transcription factors in human cancer. By functionally screening a microRNA (miR) library, we identified miR-206 as being a synthetic lethal in Myc over-expressing human cancer cells. miR-206 inhibited MAP3K13, which resulted in Myc protein de-stabilization, and an inhibition of anchorage-independent growth and in vivo tumorigenesis by Myc over-expressing human cancer cells. Eliminating MAP3K13 by shRNA recapitulated the effects caused by miR-206, thus supporting the idea that miR-206's effect on Myc was mediated through MAP3K13. Conversely, enforced expression of MAP3K13 stabilized Myc by promoting its N-terminal phosphorylation and enhancing its transcriptional activity. Gene expression analyses of breast cancers expressing high levels of Myc indicated that low miR-206 expression and high MAP3K13 expression correlated with poor patient survival. The critical link between miR-206 and MAP3K13 in the development of Myc over-expressing human cancers suggests potential points of therapeutic intervention for this molecular sub-category.
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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.