ArticleOncotarget2016
mir-101-3p is a key regulator of tumor metabolism in triple negative breast cancer targeting AMPK.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 72 citations in OpenAlex.
- MicroRNAs in Breast Cancer: Biological Functions and Technologies for Experimental and Therapeutic Applications.Cancers · 2026Review
- Integrating circulating microRNAs with epidemiological factors enhances breast cancer detection across subtypes: the MCC-Spain study.Scientific reports · 2026Article
- miR-101-3p overexpression suppresses NSCLC progression through Immune-Related gene CALCRL regulation and lncRNA NEAT1 axis.Molecular biology reports · 2025Article
- T-Cadherin (International journal of molecular sciences · 2025Review
- Circulating miRNAs signature on breast cancer: the MCC-Spain project.European journal of medical research · 2023Article
- Article
- Non-coding RNAs in breast cancer: with a focus on glucose metabolism reprogramming.Discover oncology · 2023Review
- Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer.Molecules (Basel, Switzerland) · 2023Review
- The functional significance and cross-talk of non-coding RNAs in triple negative and quadruple negative breast cancer.Molecular biology reports · 2022Review
- Epi-miRNAs: Regulators of the Histone Modification Machinery in Human Cancer.Journal of oncology · 2022Review
- microRNAs associated with the pathogenesis and their role in regulating various signaling pathways duringFrontiers in cellular and infection microbiology · 2022Review
- Natural Baicalein-Rich Fraction as Radiosensitizer in Combination with Bismuth Oxide Nanoparticles and Cisplatin for Clinical Radiotherapy.International journal of nanomedicine · 2022Article
- miR-101-5p Acts as a Tumor Suppressor in HER2-Positive Breast Cancer Cells and Improves Targeted Therapy.Breast cancer (Dove Medical Press) · 2022Article
- Muscles in Winter: The Epigenetics of Metabolic Arrest.Epigenomes · 2021Review
- Combinatorial targeting of microRNA-26b and microRNA-101 exerts a synergistic inhibition on cyclooxygenase-2 in brain metastatic triple-negative breast cancer cells.Breast cancer research and treatment · 2021Article
- Tissue-Specific Warburg Effect in Breast Cancer and Cancer-Associated Adipose Tissue-Relationship between AMPK and Glycolysis.Cancers · 2021Article
- Smooth muscle-specific HuR knockout induces defective autophagy and atherosclerosis.Cell death & disease · 2021Article
- Role of AMPK and Akt in triple negative breast cancer lung colonization.Neoplasia (New York, N.Y.) · 2021Article
- Circulating microRNAs in Early Breast Cancer Patients and Its Association With Lymph Node Metastases.Frontiers in oncology · 2021Article
- Advances in Understanding Mitochondrial MicroRNAs (mitomiRs) on the Pathogenesis of Triple-Negative Breast Cancer (TNBC).Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
mir-101-3p has been reported to be a tumor suppressor and a promising therapeutic target in cancer. Recently, AMPK dysfunction has been highlighted in cancers, including breast cancer. The aim of this study is to investigate the biological roles of mir-101-3p and AMPK in breast cancer. Our research demonstrated that AMPK was up-regulated in breast cancer tissues and cell lines, especially in triple negative breast cancer (TNBC). High-expression of AMPK correlated with poor outcome in both total breast cancer and TNBC patients. Ectopic expression of AMPK improved glucose uptake, glycolysis, proliferation of TNBC cells in vitro and its tumorigenicity in vivo. AMPK was predicted to be a direct target of mir-101-3p. The luciferase reporter assay was performed to certificate this prediction. The expression of AMPK was suppressed by transfection of mir-101-3p in TNBC cells. Over-expression of mir-101-3p or knock-down of AMPK inhibited glucose metabolism and proliferation of TNBC cells in vitro. Our study provides evidence that mir-101-3p- AMPK axis could be a promising therapeutic target in TNBC targeting tumor metabolism.
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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.