ArticleCell death & disease2017
MiR-1 suppresses tumor cell proliferation in colorectal cancer by inhibition of Smad3-mediated tumor glycolysis.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 119 citations in OpenAlex.
- The multifaceted role of microRNAs in colorectal cancer: pathogenesis and therapeutic implications.Non-coding RNA research · 2025Review
- Lactate and lactylation in tumor immunity.Frontiers of medicine · 2025Review
- Exploring miRNA Research in Colorectal Cancer: Insights from a Bibliometric Analysis.Pharmaceutics · 2025Article
- Natural compounds as regulators of miRNAs: exploring a new avenue for treating colorectal cancer.Functional & integrative genomics · 2025Review
- Unraveling the role of oligodendrocytes and myelin in pain.Journal of neurochemistry · 2025Review
- Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis.Frontiers in pharmacology · 2024Article
- Sorbitol Destroyed Intestinal Microfold Cells (M Cells) Development through Inhibition of PDE4-Mediated RANKL Expression.Mediators of inflammation · 2024Article
- Circular RNA MTCL1 targets SMAD3 by sponging miR-145-5p for regulation of cell proliferation and migration in Hirschsprung's disease.Pediatric surgery international · 2023Article
- Article
- Helicobacter pylori promotes gastric intestinal metaplasia through activation of IRF3-mediated kynurenine pathway.Cell communication and signaling : CCS · 2023Article
- An insight into the associations between microRNA expression and mitochondrial functions in cancer cell and cancer stem cell.Molecular biology reports · 2023Review
- Role of Human Monocarboxylate Transporter 1 (hMCT1) and 4 (hMCT4) in Tumor Cells and the Tumor Microenvironment.Cancer management and research · 2023Review
- Vitronectin Destroyed Intestinal Epithelial Cell Differentiation through Activation of PDE4-Mediated Ferroptosis in Inflammatory Bowel Disease.Mediators of inflammation · 2023Article
- Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells.Cell communication and signaling : CCS · 2022Article
- An integrated approach to understand fluid shear stress-driven and reactive oxygen species-mediated metastasis of colon adenocarcinoma through mRNA-miRNA-lncRNA-circRNA networks.Molecular genetics and genomics : MGG · 2022Article
- miR-1/AMPK-Mediated Glucose and Lipid Metabolism under Chronic Hypothermia in the Liver of Freshwater Drum,Metabolites · 2022Article
- MicroRNA-1: Diverse role of a small player in multiple cancers.Seminars in cell & developmental biology · 2022Review
- Propofol suppresses cell proliferation in gastric cancer cells through NRF2-mediated polyol pathway.Clinical and experimental pharmacology & physiology · 2022Article
- Vitronectin, a Novel Urinary Proteomic Biomarker, Promotes Cell Pyroptosis in Juvenile Systemic Lupus Erythematosus.Mediators of inflammation · 2022Article
- Evidence of myomiR regulation of the pentose phosphate pathway during mechanical load-induced hypertrophy.Physiological reports · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant expression of microRNA (miR)-1 has been observed in many human malignancies. However, the function and underlying mechanism of miR-1 remains elusive. To address the specific role of miR-1 in tumor glycolysis using the gain- or loss-of-function studies. Metabolic studies combined with gene expression analysis were performed in vitro and in vivo. We demonstrated aberrant expression of miR-1 in aerobic glycolysis, the Warburg effect, in cancer cells. MiR-1 suppressed aerobic glycolysis and tumor cell proliferation via inactivation of Smad3 and targeting HIF-1α, leading to reduce HK2 and MCT4 expression, which illustrated a novel pathway to mediate aerobic glycolysis in cancer cells. Overexpression of miR-1 mimics significantly decreased tumor glycolysis, including lactate production and glucose uptake, and cell proliferation, and these effects were reversed by ectopic expression of Smad3. Importantly, endogenous Smad3 regulated and interacted with HIF-1α, resulting in increasing activity of Smad3, and this interaction was dramatically abolished by addition of miR-1. We further demonstrated that Smad3 was central to the effects of miR-1 in colorectal cancer cells, establishing a previously unappreciated mechanism by which the miR-1/Smad3/HIF-1α axis facilitates the Warburg effect to promote cancer progression in vitro and in vivo. The results indicate that miR-1 may have an essential role as a tumor suppressor, suggesting its potential role in molecular therapy of patients with advanced colorectal cancer.
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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.