ArticleNature communications2020
The tumor suppressor microRNA let-7 inhibits human LINE-1 retrotransposition.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.
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Who cites it
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.
- SALL4 and microRNA: The Role of Let-7.Genes · 2021Pooled it
- The Potential Diagnostic Accuracy of Let-7 Family for Cancer: A Meta-Analysis.Technology in cancer research & treatmentPooled it
- LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- The interferon-stimulated gene product HERC5 inhibits human LINE-1 retrotransposition with an ISGylation-independent mechanism.Nucleic acids research · 2026Article
- Dynamic and Ongoing De Novo L1 Retrotransposition Contributes to Genome Plasticity and Intrapatient Heterogeneity in Ovarian Cancer.Cancer research · 2026Article
- PRICE: direct and robust detection of microRNAs at single-nucleotide resolution.Nature communications · 2026Article
- Research progress of MicroRNA in lung cancer.Discover oncology · 2026Review
- The oncogenic microRNA miR-222 promotes human LINE-1 retrotransposition.RNA biology · 2025Article
- Role of miRNAs, miR-135b-5p & miR-21-5p in metastasis of cervical cancer.The Indian journal of medical research · 2025Article
- Transposable elements in health and disease: Molecular basis and clinical implications.Chinese medical journal · 2025Review
- LINE1 insertion into the NACC2 locus disrupts the HDM2 axis and activates lung oncogenic signaling.NPJ precision oncology · 2025Article
- Regulatory Effects ofFood science & nutrition · 2025Article
- DGCR8 haploinsufficiency leads to primate-specific RNA dysregulation and pluripotency defects.Nucleic acids research · 2025Article
- Multi-ancestry GWAS reveals loci linked to human variation in LINE-1- and Alu-insertion numbers.bioRxiv : the preprint server for biology · 2025Article
- Deep Learning for Cancer Detection Based on Genomic and Imaging Data: A Comprehensive Review.Cancer management and research · 2025Review
- Multi-ancestry GWAS reveals loci linked to human variation in LINE-1- and Alu-insertion numbers.Translational medicine of aging · 2025Article
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- Recent Advances and Prospects of Nucleic Acid Therapeutics for Anti-Cancer Therapy.Molecules (Basel, Switzerland) · 2024Review
- Structural basis for activity switching in polymerases determining the fate of let-7 pre-miRNAs.Nature structural & molecular biology · 2024Article
- Non-coding RNAs as therapeutic targets in cancer and its clinical application.Journal of pharmaceutical analysis · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nearly half of the human genome is made of transposable elements (TEs) whose activity continues to impact its structure and function. Among them, Long INterspersed Element class 1 (LINE-1 or L1) elements are the only autonomously active TEs in humans. L1s are expressed and mobilized in different cancers, generating mutagenic insertions that could affect tumor malignancy. Tumor suppressor microRNAs are ∼22nt RNAs that post-transcriptionally regulate oncogene expression and are frequently downregulated in cancer. Here we explore whether they also influence L1 mobilization. We show that downregulation of let-7 correlates with accumulation of L1 insertions in human lung cancer. Furthermore, we demonstrate that let-7 binds to the L1 mRNA and impairs the translation of the second L1-encoded protein, ORF2p, reducing its mobilization. Overall, our data reveals that let-7, one of the most relevant microRNAs, maintains somatic genome integrity by restricting L1 retrotransposition.
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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.