ArticleNature communications2019
MiR-135 suppresses glycolysis and promotes pancreatic cancer cell adaptation to metabolic stress by targeting phosphofructokinase-1.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 4 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
81 citing papers in PubMed, 4 syntheses or guidelines pooled it, 132 citations in OpenAlex.
- The expression profiles and roles of microRNAs in cardiac glucose metabolism.Frontiers in endocrinology · 2025Pooled it
- Aberrant Energy Metabolism in Tumors and Potential Therapeutic Targets.Genes, chromosomes & cancer · 2024Pooled it
- Current hotspots and trends in cancer metabolic reprogramming: a scientometric analysis.Frontiers in immunology · 2024Pooled it
- Prognostic significance of microRNA-135 in patients with digestive system cancers: a systematic review and meta-analysis.Bioscience reports · 2019Pooled it
- MicroRNA-15a/16 regulate protein metabolism and are associated with clinical outcomes in pancreatic ductal adenocarcinoma.Physiological reports · 2026Article
- FragmentFinder-a user-friendly, Windows-based tool for identifying and characterizing short RNAs excised from any noncoding RNA.NAR genomics and bioinformatics · 2026Article
- Cyclin B2 facilitates glycolysis and tumor progression in pancreatic ductal adenocarcinoma by promoting histone lactylation.BMC cancer · 2025Article
- Functional requirements of the liver isoform of phosphofructokinase-1 in breast cancer cell migration.Journal of cell science · 2025Article
- Unraveling the therapeutic landscape of miRNAs in pancreatic cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Glutamine synthetase shields triple-negative breast cancer cells from ferroptosis in metastasis triggered by glutamine deprivation.Breast cancer research : BCR · 2025Article
- Decoding the pancreatic cancer microenvironment: The multifaceted regulation of microRNAs.Clinical and translational medicine · 2025Review
- The Construction of ceRNA Regulatory Network Unraveled Prognostic Biomarkers and Repositioned Drug Candidates for the Management of Pancreatic Ductal Adenocarcinoma.Current issues in molecular biology · 2025Article
- Targeted mitochondrial therapy for pancreatic cancer.Translational oncology · 2025Review
- Reprogramming of glucose metabolism in pancreatic cancer: mechanisms, implications, and therapeutic perspectives.Frontiers in immunology · 2025Review
- Glutamine's double-edged sword: fueling tumor growth and offering therapeutic hope.Frontiers in immunology · 2025Review
- Reprogramming of Glucose Metabolism by Nanocarriers to Improve Cancer Immunotherapy: Recent Advances and Applications.International journal of nanomedicine · 2025Review
- Transcriptional regulation and post-translational modifications in the glycolytic pathway for targeted cancer therapy.Acta pharmacologica Sinica · 2024Review
- Targeting cellular adaptive responses to glutaminolysis perturbation for cancer therapy.Molecules and cells · 2024Review
- miRNAs in pancreatic cancer progression and metastasis.Clinical & experimental metastasis · 2024Review
- Nutrient restriction-activated Fra-2 promotes tumor progression via IGF1R in miR-15a downmodulated pancreatic ductal adenocarcinoma.Signal transduction and targeted therapy · 2024Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human cancers. It thrives in a nutrient-poor environment; however, the mechanisms by which PDAC cells undergo metabolic reprogramming to adapt to metabolic stress are still poorly understood. Here, we show that microRNA-135 is significantly increased in PDAC patient samples compared to adjacent normal tissue. Mechanistically, miR-135 accumulates specifically in response to glutamine deprivation and requires ROS-dependent activation of mutant p53, which directly promotes miR-135 expression. Functionally, we found miR-135 targets phosphofructokinase-1 (PFK1) and inhibits aerobic glycolysis, thereby promoting the utilization of glucose to support the tricarboxylic acid (TCA) cycle. Consistently, miR-135 silencing sensitizes PDAC cells to glutamine deprivation and represses tumor growth in vivo. Together, these results identify a mechanism used by PDAC cells to survive the nutrient-poor tumor microenvironment, and also provide insight regarding the role of mutant p53 and miRNA in pancreatic cancer cell adaptation to metabolic stresses.
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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.