ArticleNature communications2022
Long noncoding RNA DIO3OS induces glycolytic-dominant metabolic reprogramming to promote aromatase inhibitor resistance in breast cancer.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- A systematic review of progress toward unlocking the power of epigenetics in breast cancer: latest updates and perspectives.Frontiers in pharmacology · 2025Pooled it
- Research progresses and hotspots on glucose metabolic reprogramming in breast cancer: a bibliometric analysis over the past two decades.Frontiers in oncology · 2024Pooled it
- RUNX2 promotes osteoclast differentiation and bone resorption via the newly identified LncRNA-ROD: implications for alveolar remodeling.International journal of oral science · 2026Article
- Article
- Long non-coding RNAs as modulators of endocrine therapy response in hormone receptor-positive breast cancer.Molecular biology reports · 2026Review
- Oncogenic functions of polypyrimidine tract-binding protein 1 in breast cancer metabolism and progression.Biochemistry and biophysics reports · 2026Article
- MTUS2-AS1 suppression promotes DDX5 protein degradation to enhance the sensitivity of PARP inhibitors in BRCA-wild triple negative breast cancer.International journal of biological sciences · 2026Article
- Exploring exosomal lncRNAs: unlocking the molecular code of tumor metastasis and drug resistance.Cancer cell international · 2025Review
- The role of UPR-related long noncoding RNAs in development of endocrine resistance in breast cancer.International journal of cancer · 2025Review
- Long non-coding RNAs in cancer glycolysis and metabolism: mechanisms and translational opportunities.Cell death & disease · 2025Review
- LINC01198 activates Hippo signaling to stimulate IL-1β autocrine for driving vemurafenib resistance by associating with TAOK1/2 in melanoma.Cell death discovery · 2025Article
- Review
- Female and male hormonal-dependent malignancies: the role of long non-coding RNAs.Medical oncology (Northwood, London, England) · 2025Review
- Increasing linc00261 expression may predict well cancer prognosis, based on the meta-analysis.Discover oncology · 2025Review
- Targeting ncRNAs to overcome metabolic reprogramming‑mediated drug resistance in cancer (Review).International journal of oncology · 2025Review
- Warburg effect and lactylation in cancer: mechanisms for chemoresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
- Regulation of Glycolysis by SMAD5 in Glioma Cells: Implications for Tumor Growth and Apoptosis.Neurochemical research · 2025Article
- Long Non-Coding RNAs: Key Regulators of Tumor Epithelial/Mesenchymal Plasticity and Cancer Stemness.Cells · 2025Review
- MNX1-AS1 suppresses chemosensitivity by activating the PI3K/AKT pathway in breast cancer.International journal of biological sciences · 2025Article
- Role of Long Noncoding RNA Dio3os in Glycolipid Metabolism.Current genomics · 2025Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aromatase inhibition is an efficient endocrine therapy to block ectopic estrogen production for postmenopausal estrogen receptor (ER)-positive breast cancer patients, but many develop resistance. Here, we show that aromatase inhibitor (AI)-resistant breast tumors display features of enhanced aerobic glycolysis with upregulation of long noncoding RNA (lncRNA) DIO3OS, which correlates with poor prognosis of breast cancer patients on AI therapies. Long-term estrogen deprivation induces DIO3OS expression in ER-positive breast tumor cells, which further enhances aerobic glycolysis and promotes estrogen-independent cell proliferation in vitro and in vivo. Mechanistically, DIO3OS interacts with polypyrimidine tract binding protein 1 (PTBP1) and stabilizes the mRNA of lactate dehydrogenase A (LDHA) by protecting the integrity of its 3'UTR, and subsequently upregulates LDHA expression and activates glycolytic metabolism in AI-resistant breast cancer cells. Our findings highlight the role of lncRNA in regulating the key enzyme of glycolytic metabolism in response to endocrine therapies and the potential of targeting DIO3OS to reverse AI resistance in ER-positive breast cancer.
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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.