ArticleCell cycle (Georgetown, Tex.)2016
lncRNA NBR2 modulates cancer cell sensitivity to phenformin through GLUT1.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 74 citations in OpenAlex.
- Phenformin-Induced Apoptosis: A Potential Mechanism for Cervical Cancer Cell Inhibition.International journal of molecular sciences · 2026Article
- LncRNA NBR2 affects pancreatic β-cell function in type 2 diabetes mellitus by targeting miR-646.Diabetology & metabolic syndrome · 2025Article
- Decoding BRCA1 promoter hypermethylation: a new frontier in understanding sporadic breast cancer.Cancer gene therapy · 2025Article
- The role of curcumin in modulating circular RNAs and long non-coding RNAs in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Nuclear-activating miRNAs: unveiling the intricacies of subcellular miRNA function and regulation in cancer and immunity disease.Cancer cell international · 2025Review
- Proteomic analysis of ferroptosis pathways reveals a role of CEPT1 in suppressing ferroptosis.Protein & cell · 2024Article
- BRCA1-Mediated Dual Regulation of Ferroptosis Exposes a Vulnerability to GPX4 and PARP Co-Inhibition in BRCA1-Deficient Cancers.Cancer discovery · 2024Article
- IRE1α determines ferroptosis sensitivity through regulation of glutathione synthesis.Nature communications · 2024Article
- The m6A modification-mediated positive feedback between glycolytic lncRNA SLC2A1-DT and c-Myc promotes tumorigenesis of hepatocellular carcinoma.International journal of biological sciences · 2024Article
- SLC7A11 expression level dictates differential responses to oxidative stress in cancer cells.Nature communications · 2023Article
- Decoding the regulatory roles of non-coding RNAs in cellular metabolism and disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Functional importance of glucose transporters and chromatin epigenetic factors in Glioblastoma Multiforme (GBM): possible therapeutics.Metabolic brain disease · 2023Review
- Cuproptosis-related lncRNAs forecast the prognosis of acute myeloid leukemia.Translational cancer research · 2023Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis.Nature cell biology · 2023Article
- A ferroptosis defense mechanism mediated by glycerol-3-phosphate dehydrogenase 2 in mitochondria.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A targetable CoQ-FSP1 axis drives ferroptosis- and radiation-resistance in KEAP1 inactive lung cancers.Nature communications · 2022Article
- Piperlongumine, a piper alkaloid, enhances the efficacy of doxorubicin in breast cancer: involvement of glucose import, ROS, NF-κB and lncRNAs.Apoptosis : an international journal on programmed cell death · 2022Article
- The Epithelial-Mesenchymal Transition at the Crossroads between Metabolism and Tumor Progression.International journal of molecular sciences · 2022Review
- Long non-coding RNAs play an important regulatory role in tumorigenesis and tumor progression through aerobic glycolysis.Frontiers in molecular biosciences · 2022Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Biguanides, including metformin (widely used in diabetes treatment) and phenformin, are AMP-activated protein kinase (AMPK) activators and potential drugs for cancer treatment. A more in-depth understanding of how cancer cells adapt to biguanide treatment may provide important therapeutic implications to achieve more effective and rational cancer therapies. NBR2 is a glucose starvation-induced long non-coding RNA (lncRNA) that interacts with AMPK and regulates AMPK activity upon glucose starvation. Here we show that phenformin treatment induces NBR2 expression, and NBR2 deficiency sensitizes cancer cells to phenformin-induced cell death. Surprisingly, unlike glucose starvation, phenformin does not induce NBR2 interaction with AMPK, and correspondingly, NBR2 deficiency does not affect phenformin-induced AMPK activation. We further reveal that NBR2 depletion attenuates phenformin-induced glucose transporter GLUT1 expression and glucose uptake. GLUT1 deficiency sensitizes cancer cells to phenformin-induced cell death, whereas GLUT1 restoration in NBR2 deficient cells rescues the increased cell death upon phenformin treatment. Together, the results of our study reveal that NBR2-GLUT1 axis may serve as an adaptive response in cancer cells to survive in response to phenformin treatment, and identify a novel mechanism coupling lncRNA to biguanide-mediated biology.
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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 Socratic graph.