ArticleOncotarget2015
Metabolic reprogramming of metastatic breast cancer and melanoma by let-7a microRNA.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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.
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Who cites it
44 citing papers in PubMed, 77 citations in OpenAlex.
- Predicting and understanding the response to short-term intensive insulin therapy in people with early type 2 diabetes.Molecular metabolism · 2019Trial
- Lin28/let-7 axis in breast cancer.Molecular biology reports · 2025Review
- Non-metabolic enzyme function of pyruvate kinase M2 in breast cancer.Frontiers in oncology · 2024Review
- A Journey to Reach the Ovary Using Next-Generation Technologies.International journal of molecular sciences · 2023Review
- Non-coding RNAs in breast cancer: with a focus on glucose metabolism reprogramming.Discover oncology · 2023Review
- MiRNAs Action and Impact on Mitochondria Function, Metabolic Reprogramming and Chemoresistance of Cancer Cells: A Systematic Review.Biomedicines · 2023Review
- The role of LIN28B in tumor progression and metastasis in solid tumor entities.Oncology research · 2023Review
- The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role.Molecular cancer · 2022Review
- The Metabolism Reprogramming of microRNA Let-7-Mediated Glycolysis Contributes to Autophagy and Tumor Progression.International journal of molecular sciences · 2021Review
- Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4.Cancer cell international · 2021Article
- MitomiRs: their roles in mitochondria and importance in cancer cell metabolism.Radiology and oncology · 2021Review
- Let-7a-5p, miR-100-5p, miR-101-3p, and miR-199a-3p Hyperexpression as Potential Predictive Biomarkers in Early Breast Cancer Patients.Journal of personalized medicine · 2021Article
- Review
- Up-regulation of KISS1 as a novel target of Let-7i in melanoma serves as a potential suppressor of migration and proliferation in vitro.Journal of cellular and molecular medicine · 2021Article
- Reciprocal Changes in miRNA Expression with Pigmentation and Decreased Proliferation Induced in Mouse B16F1 Melanoma Cells by L-Tyrosine and 5-Bromo-2'-Deoxyuridine.International journal of molecular sciences · 2021Article
- Advances in Understanding Mitochondrial MicroRNAs (mitomiRs) on the Pathogenesis of Triple-Negative Breast Cancer (TNBC).Oxidative medicine and cellular longevity · 2021Review
- Revisiting cancer hallmarks: insights from the interplay between oxidative stress and non-coding RNAs.Molecular biomedicine · 2020Review
- Review
- The Regulatory Role of Mitochondrial MicroRNAs (MitomiRs) in Breast Cancer: Translational Implications Present and Future.Cancers · 2020Review
- Anti-Angiogenic Effects of Phytochemicals on miRNA Regulating Breast Cancer Progression.Biomolecules · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Let-7 microRNAs (miRNAs) are highly conserved well-established promoters of terminal differentiation that are expressed in healthy adult tissues and frequently repressed in cancer cells. The tumor suppressive role of let-7 in a variety of cancers in vitro and in vivo has been widely documented and prompted these miRNAs to be candidate genes for miRNA replacement therapy. In this study we described a new role of let-7a in reprogramming cancer metabolism, recently identified as a new hallmark of cancer. We show that let-7a down-regulates key anabolic enzymes and increases both oxidative phosphorylation and glycolysis in triple-negative breast cancer and metastatic melanoma cell lines. Strikingly, the accelerated glycolysis coexists with drastically reduced cancer features. Moreover, let-7a causes mitochondrial ROS production concomitant with the up-regulation of oxidative stress responsive genes. To exploit these increased ROS levels for therapeutic purposes, we combined let-7a transfection with the chemotherapeutic drug doxorubicin. In both cancer types let-7a increased cell sensitivity to doxorubicin. Pre-treatment with N-acetyl cysteine (NAC) totally abolished this effect, indicating that the increased doxorubicin sensitivity of let-7a cells depends on the redox pathway. We thus have demonstrated that let-7a plays a prominent role in regulating energy metabolism in cancer cells, further expanding its therapeutic potential.
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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.