ArticleThe Journal of biological chemistry2011
MYC protein inhibits transcription of the microRNA cluster MC-let-7a-1~let-7d via noncanonical E-box.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- The microRNA Let-7 and its exosomal form: Epigenetic regulators of gynecological cancers.Cell biology and toxicology · 2024Review
- Exploring non-coding RNA mechanisms in hepatocellular carcinoma: implications for therapy and prognosis.Frontiers in immunology · 2024Review
- Emerging role of MicroRNA-Based theranostics in Hepatocellular Carcinoma.Molecular biology reports · 2023Review
- MicroRNA Profiling Shows a Time-Dependent Regulation within the First 2 Months Post-Birth and after Mild Neonatal Hypoxia in the Hippocampus from Mice.Biomedicines · 2022Article
- Oxidative Stress and Inflammation in Cardiovascular Diseases and Cancer: Role of Non-coding RNAs.The Yale journal of biology and medicine · 2022Review
- The Role of microRNA Let-7d in Female Malignancies and Diseases of the Female Reproductive Tract.International journal of molecular sciences · 2021Review
- Review
- The Epithelial-Mesenchymal Transcription FactorCancers · 2021Article
- Association between microRNA-527 and glypican-3 in hepatocellular carcinoma.Oncology letters · 2021Article
- Review
- microRNA cluster MC-let-7a-1~let-7d promotes autophagy and apoptosis of glioma cells by down-regulating STAT3.CNS neuroscience & therapeutics · 2020Article
- MicroRNAs Targeting MYC Expression: Trace of Hope for Pancreatic Cancer Therapy. A Systematic Review.Cancer management and research · 2020Review
- Let-7 as biomarker, prognostic indicator, and therapy for precision medicine in cancer.Clinical and translational medicine · 2019Review
- A Regulator of Metabolic Reprogramming: MicroRNA Let-7.Translational oncology · 2019Article
- Preliminary study on the effect of nucleolin specific aptamer-miRNA let-7d chimera on Janus kinase-2 expression level and activity in gastric cancer (MKN-45) cells.Molecular biology reports · 2019Article
- Role of tumor-associated neutrophils in regulation of tumor growth in lung cancer development: A mathematical model.PloS one · 2019Article
- LIN28 Selectively Modulates a Subclass of Let-7 MicroRNAs.Molecular cell · 2018Article
- Different levels of let-7d expression modulate response of FaDu cells to irradiation and chemotherapeutics.PloS one · 2017Article
- Animal Models to Study MicroRNA Function.Advances in cancer research · 2017Review
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human microRNA cluster MC-let-7a-1∼let-7d, with three members let-7a-1, let-7f-1, and let-7d, is an important cluster of the let-7 family. These microRNAs play critical roles in regulating development and carcinogenesis. Therefore, precise control of MC-let-7a-1∼let-7d level is critical for cellular functions. In this study, we first showed that the expression of these three members was significantly reduced in human hepatocellular carcinoma HepG2 cells as compared with the immortalized human liver L02 cells. We demonstrated that the MC-let-7a-1∼let-7d cluster was encoded by a single polycistronic transcript driven by a 10-kb upstream promoter, with two MYC-binding sites. Importantly, MYC inhibited MC-let-7a-1∼let-7d promoter activity via binding to the noncanonical E-box 3 downstream of the transcription start sites, whereas it enhanced promoter activity by binding to the canonical E-box 2 upstream of the transcription start sites. We found that although the binding affinity of MYC to E-box 2 was stronger than E-box 3, the binding quantum of MYC to E-box 3 was significantly higher in cancerous HepG2 cells as compared with the noncancerous L02 cells. In addition, forced expression of let-7 could reverse the MYC-mediated cell proliferation. These findings suggested that in L02 cells with a low level of MYC, MYC binds mainly to E-box 2 to enhance MC-let-7a-1∼let-7d expression. However, in HepG2 cells with an elevated MYC, the extra MYC could bind to E-box 3 to suppress the transcription of MC-let-7a-1∼let-7d and thus enable HepG2 cells to maintain a high level of MYC and a low level of let-7 microRNAs simultaneously.
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