ArticleeLife2015
Precise let-7 expression levels balance organ regeneration against tumor suppression.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- The Long Non-Coding RNA SNHG16 Negatively Regulates Let-7 and Predicts Recurrence in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Article
- A Novel Role for the Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Delta Isoform in Hepatocellular Proliferation.The American journal of pathology · 2024Article
- Engineered extracellular vesicles carrying let-7a-5p for alleviating inflammation in acute lung injury.Journal of biomedical science · 2024Article
- Pharmacological inhibition of Lin28 promotes ketogenesis and restores lipid homeostasis in models of non-alcoholic fatty liver disease.Nature communications · 2022Article
- Lipid Nanoparticle (LNP) Chemistry Can Endow UniqueMolecular pharmaceutics · 2022Article
- Let-7 as a Promising Target in Aging and Aging-Related Diseases: A Promise or a Pledge.Biomolecules · 2022Review
- Tumor-targeted miRNA nanomedicine for overcoming challenges in immunity and therapeutic resistance.Nanomedicine (London, England) · 2022Review
- Let-7 underlies metformin-induced inhibition of hepatic glucose production.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Non-microRNA binding competitively inhibits LIN28 regulation.Cell reports · 2021Article
- MicroRNA Let-7 targets AMPK and impairs hepatic lipid metabolism in offspring of maternal obese pregnancies.Scientific reports · 2021Article
- Functional Characterization of the Lin28/let-7 Circuit During Forelimb Regeneration inFrontiers in cell and developmental biology · 2020Article
- Article
- Roles of mTOR Signaling in Tissue Regeneration.Cells · 2019Review
- Let-7 as biomarker, prognostic indicator, and therapy for precision medicine in cancer.Clinical and translational medicine · 2019Review
- Dual mechanisms of posttranscriptional regulation of Tet2 by Let-7 microRNA in macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Targeting LIN28B reprograms tumor glucose metabolism and acidic microenvironment to suppress cancer stemness and metastasis.Oncogene · 2019Article
- Modulation of TNFα Activity by the microRNA Let-7 Coordinates Zebrafish Heart Regeneration.iScience · 2019Article
- Exportin-T promotes tumor proliferation and invasion in hepatocellular carcinoma.Molecular carcinogenesis · 2019Article
- C/EBPβ-LIP induces cancer-type metabolic reprogramming by regulating theCommunications biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
Abstract
The in vivo roles for even the most intensely studied microRNAs remain poorly defined. Here, analysis of mouse models revealed that let-7, a large and ancient microRNA family, performs tumor suppressive roles at the expense of regeneration. Too little or too much let-7 resulted in compromised protection against cancer or tissue damage, respectively. Modest let-7 overexpression abrogated MYC-driven liver cancer by antagonizing multiple let-7 sensitive oncogenes. However, the same level of overexpression blocked liver regeneration, while let-7 deletion enhanced it, demonstrating that distinct let-7 levels can mediate desirable phenotypes. let-7 dependent regeneration phenotypes resulted from influences on the insulin-PI3K-mTOR pathway. We found that chronic high-dose let-7 overexpression caused liver damage and degeneration, paradoxically leading to tumorigenesis. These dose-dependent roles for let-7 in tissue repair and tumorigenesis rationalize the tight regulation of this microRNA in development, and have important implications for let-7 based therapeutics.
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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.