ArticleScientific reports2018
Loss of function of miR-342-3p results in MCT1 over-expression and contributes to oncogenic metabolic reprogramming in triple negative breast cancer.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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69 citing papers in PubMed, 98 citations in OpenAlex.
- Metastasis of triple negative breast cancer is regulated by a targetable miR-342-E2F network.EMBO molecular medicine · 2026Article
- Extracellular vesicles in nipple discharge for breast cancer screening.Breast cancer research and treatment · 2026Article
- Noncoding RNAs in Metabolic Reprogramming of Breast Cancer: Dietary Opportunities and Translational Implications.Experientia supplementum (2012) · 2026Review
- Intronic miR-342 is a key regulator of cellular glycolysis in Foxp3+ regulatory CD4 T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Lactate and lactylation in tumor immunity.Frontiers of medicine · 2025Review
- The pleiotropic roles of non-hormonal receptor basigin and regulatory microRNAs in breast cancer.NPJ breast cancer · 2025Review
- Peripheral blood miRNAs are associated with airflow below threshold in children with asthma.Respiratory research · 2025Article
- Article
- Emodin regulated lactate metabolism by inhibiting MCT1 to delay non-small cell lung cancer progression.Human cell · 2024Article
- Micro-RNAs in breast cancer progression and metastasis: A chromatin and metabolic perspective.Heliyon · 2024Review
- Transcriptional regulation and post-translational modifications in the glycolytic pathway for targeted cancer therapy.Acta pharmacologica Sinica · 2024Review
- MicroRNAs as promising biomarkers and potential therapeutic agents in breast cancer management: a comprehensive review.Annals of medicine and surgery (2012) · 2024Review
- An evolutionary learning-based method for identifying a circulating miRNA signature for breast cancer diagnosis prediction.NAR genomics and bioinformatics · 2024Article
- Elucidating the molecular basis of ATP-induced cell death in breast cancer: Construction of a robust prognostic model.World journal of clinical oncology · 2024Article
- A gene expression-based classifier for HER2-low breast cancer.Scientific reports · 2024Article
- Inhibitory effect of miR342 on the progression of triple-negative breast cancer cells in vitro and in the mice model.BioImpacts : BI · 2024Article
- MicroRNA dysregulation in ataxia telangiectasia.Frontiers in immunology · 2024Article
- The Pivotal Function of SLC16A1 and SLC16A1-AS1 in Cancer Progress: Molecular Pathogenesis and Prognosis.Mini reviews in medicinal chemistry · 2024Article
- miRNA-Based Technologies in Cancer Therapy.Journal of personalized medicine · 2023Review
- Identification of a serum-based microRNA signature that detects recurrent oral squamous cell carcinoma before it is clinically evident.British journal of cancer · 2023Article
9 more citing papers are in PubMed but not listed here.
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9 authors at 2 institutions in 2 countries.
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Abstract
Triple-negative breast cancer (TNBC) is a heterogeneous and aggressive neoplasia lacking the expression of hormonal receptors and human epidermal growth factor receptor-2. Accumulating evidence has highlighted the importance of miRNAs dysregulation in the establishment of cancer programs, but the functional role of many miRNAs remains unclear. The description of miRNAs roles might provide novel strategies for treatment. In the present work, an integrated analysis of miRNA transcriptional landscape was performed (N = 132), identifying the significant down-modulation of miR-342-3p in TNBC, probably because of the aberrant activity of estrogen receptor, which serves as a transcription factor of the miRNA, as demonstrated by a siRNA-knockdown approach. The enhanced expression of miR-342-3p significantly decreased cell proliferation, viability and migration rates of diverse TN cells in vitro. Bioinformatic and functional analyses revealed that miR-342-3p directly targets the monocarboxylate transporter 1 (MCT1), which promotes lactate and glucose fluxes alteration, thus disrupting the metabolic homeostasis of tumor cells. Optical metabolic imaging assay defined a higher optical redox ratio in glycolytic cells overexpressing miR-342-3p. Furthermore, we found that hypoxic conditions and glucose starvation attenuate miR-342-3p expression, suggesting a crosstalk program between these metabolic factors. Consistently, miR-342-3p down-modulation is associated with an increased MCT1 expression level and glycolytic score in human triple negative tumors. Overall, we described for the first time the regulatory activity of miR-342-3p on relevant metabolic carcinogenic pathways in TN breast cancers.
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