ArticleNature2016
Multiple mechanisms disrupt the let-7 microRNA family in neuroblastoma.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 181 citations in OpenAlex.
- The PLK4 inhibitor RP-1664 demonstrates potent efficacy in neuroblastoma preclinical models through a dual mechanism of sensitivity.Nature communications · 2026Article
- PRICE: direct and robust detection of microRNAs at single-nucleotide resolution.Nature communications · 2026Article
- Targeting the Lin28/let-7 Axis with Compounds to Regulate Transcriptional Control in Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- CRISPR/Cas9 in cancer therapy: clinical translation, mechanistic strategies, and therapeutic directions.Frontiers in oncology · 2026Review
- LIN28-mediated gene regulatory loops synchronize transitions throughout organogenesis.Biochemistry and biophysics reports · 2025Article
- Extracellular vesicle derived miRNAs from plasma as promising diagnosis and prognosis biomarkers for neuroblastoma.iScience · 2025Article
- The Non-Coding Regulatory Variant rs2863002 at chr11p11.2 Increases Neuroblastoma Risk by Affecting HSD17B12 Expression and Lipid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Regulation and dysregulation of microRNA - transcription factor axes in differentiation and neuroblastoma.Cellular and molecular life sciences : CMLS · 2025Review
- Emerging clinical and research approaches in targeted therapies for high-risk neuroblastoma.Frontiers in oncology · 2025Review
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- Pleiotropic GeneAnimals : an open access journal from MDPI · 2024Article
- Structural basis for activity switching in polymerases determining the fate of let-7 pre-miRNAs.Nature structural & molecular biology · 2024Article
- Profile of miRNA expression in the hippocampus of epileptic mice and the prediction of potential therapeutic targets.Molecular biology reports · 2024Article
- Unsaturated Fatty Acid Synthesis Is Associated with Worse Survival and Is Differentially Regulated byCancers · 2024Article
- N-MYC regulates cell survival via eIF4G1 in inv(16) acute myeloid leukemia.Science advances · 2024Article
- Epigenetic Dysregulation inInternational journal of molecular sciences · 2023Review
- Article
- A MYCN-independent mechanism mediating secretome reprogramming and metastasis inScience advances · 2023Article
- Review
- Small regulatory RNAs: from bench to bedside - a keystone symposia meeting report.RNA biology · 2023Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Poor prognosis in neuroblastoma is associated with genetic amplification of MYCN. MYCN is itself a target of let-7, a tumour suppressor family of microRNAs implicated in numerous cancers. LIN28B, an inhibitor of let-7 biogenesis, is overexpressed in neuroblastoma and has been reported to regulate MYCN. Here we show, however, that LIN28B is dispensable in MYCN-amplified neuroblastoma cell lines, despite de-repression of let-7. We further demonstrate that MYCN messenger RNA levels in amplified disease are exceptionally high and sufficient to sponge let-7, which reconciles the dispensability of LIN28B. We found that genetic loss of let-7 is common in neuroblastoma, inversely associated with MYCN amplification, and independently associated with poor outcomes, providing a rationale for chromosomal loss patterns in neuroblastoma. We propose that let-7 disruption by LIN28B, MYCN sponging, or genetic loss is a unifying mechanism of neuroblastoma development with broad implications for cancer pathogenesis.
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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.