ArticleScientific reports2017
Disrupting glutamine metabolic pathways to sensitize gemcitabine-resistant pancreatic cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 99 citations in OpenAlex.
- Untargeted Metabolomics Analysis Reveals Potential Metabolic Targets in Gemcitabine-Treated Pancreatic Cancer Cells.Metabolites · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Sugar symphony: glycosylation in cancer metabolism and stemness.Trends in cell biology · 2025Review
- Targeted mitochondrial therapy for pancreatic cancer.Translational oncology · 2025Review
- Exploring the potential of gemcitabine-metal-organic frameworks in combating pancreatic cancer under ketogenic conditions.BMC cancer · 2025Article
- Oncometabolites in pancreatic cancer: Strategies and its implications.World journal of experimental medicine · 2024Review
- The Role of Dicer Phosphorylation in Gemcitabine Resistance of Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Article
- Metabolic responses to the occurrence and chemotherapy of pancreatic cancer: biomarker identification and prognosis prediction.Scientific reports · 2024Article
- A stumbling block in pancreatic cancer treatment: drug resistance signaling networks.Frontiers in cell and developmental biology · 2024Review
- Glutamine addiction and therapeutic strategies in pancreatic cancer.World journal of gastrointestinal oncology · 2023Review
- Monocarboxylate Transporter-1 (MCT1)-Mediated Lactate Uptake Protects Pancreatic Adenocarcinoma Cells from Oxidative Stress during Glutamine Scarcity Thereby Promoting Resistance against Inhibitors of Glutamine Metabolism.Antioxidants (Basel, Switzerland) · 2023Article
- HIF2α, Hepcidin and their crosstalk as tumour-promoting signalling.British journal of cancer · 2023Review
- The coagulation-related genes for prognosis and tumor microenvironment in pancreatic ductal adenocarcinoma.BMC cancer · 2023Article
- Metabolic Rewiring and Stemness: A Critical Attribute of Pancreatic Cancer Progression.Stem cells (Dayton, Ohio) · 2023Review
- Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies.Metabolites · 2023Review
- ARPC1A correlates with poor prognosis in prostate cancer and is up-regulated by glutamine metabolism to promote tumor cell migration, invasion and cytoskeletal changes.Cell & bioscience · 2023Article
- Mitochondrial Metabolism in Pancreatic Ductal Adenocarcinoma: From Mechanism-Based Perspectives to Therapy.Cancers · 2023Review
- Article
- Mucin 4 Confers Gemcitabine Resistance and an Unfavorable Prognosis in Patients with Cholangiocarcinoma via AKT Activation.International journal of biological sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic cancer is a lethal disease with poor prognosis. Gemcitabine has been the first line systemic treatment for pancreatic cancer. However, the rapid development of drug resistance has been a major hurdle in gemcitabine therapy leading to unsatisfactory patient outcomes. With the recent renewed understanding of glutamine metabolism involvement in drug resistance and immuno-response, we investigated the anti-tumor effect of a glutamine analog (6-diazo-5-oxo-L-norleucine) as an adjuvant treatment to sensitize chemoresistant pancreatic cancer cells. We demonstrate that disruption of glutamine metabolic pathways improves the efficacy of gemcitabine treatment. Such a disruption induces a cascade of events which impacts glycan biosynthesis through Hexosamine Biosynthesis Pathway (HBP), as well as cellular redox homeostasis, resulting in global changes in protein glycosylation, expression and functional effects. The proteome alterations induced in the resistant cancer cells and the secreted exosomes are intricately associated with the reduction in cell proliferation and the enhancement of cancer cell chemosensitivity. Proteins associated with EGFR signaling, including downstream AKT-mTOR pathways, MAPK pathway, as well as redox enzymes were downregulated in response to disruption of glutamine metabolic pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.