ArticleCells2023
Resistance to Gemcitabine in Pancreatic Cancer Is Connected to Methylglyoxal Stress and Heat Shock Response.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Turning off methylglyoxal stress: an alternative approach to inhibit MDSC expansion and metastasis in triple-negative breast cancer.Journal for immunotherapy of cancer · 2026Article
- Heat Shock Proteins as Cancer Biomarkers: From Mechanism to Clinical Application.Molecular diagnosis & therapy · 2026Review
- Deciphering the mechanisms by which probioticCurrent research in food science · 2026Article
- Inhibition of C5a-C5aR1 axis suppresses tumour progression by enhancing antitumour immunity and chemotherapeutic effect in pancreatic ductal adenocarcinoma.British journal of cancer · 2025Article
- A comprehensive pan-cancer analysis of the prognostic role and immunotherapy efficacy evaluation of Glyoxalase 1.Discover oncology · 2025Article
- Heat Shock Proteins in Pancreatic Cancer: Pathogenic Mechanisms and Clinical Implications.Cells · 2025Review
- Lactate dehydrogenase A: a potential new target for tumor drug resistance intervention.Journal of translational medicine · 2025Review
- Exploring the potential of gemcitabine-metal-organic frameworks in combating pancreatic cancer under ketogenic conditions.BMC cancer · 2025Article
- Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025Review
- Integrating plasma protein-centric multi-omics to identify potential therapeutic targets for pancreatic cancer.Journal of translational medicine · 2024Article
- Establishment and characterization of the gemcitabine-resistant human gallbladder cancer cell line NOZ GemR.Annals of medicine and surgery (2012) · 2024Article
- The small-molecule drug homoharringtonine targets HSF1 to suppress pancreatic cancer progression.American journal of cancer research · 2024Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with poor prognosis. Gemcitabine is the first-line therapy for PDAC, but gemcitabine resistance is a major impediment to achieving satisfactory clinical outcomes. This study investigated whether methylglyoxal (MG), an oncometabolite spontaneously formed as a by-product of glycolysis, notably favors PDAC resistance to gemcitabine. We observed that human PDAC tumors expressing elevated levels of glycolytic enzymes together with high levels of glyoxalase 1 (GLO1), the major MG-detoxifying enzyme, present with a poor prognosis. Next, we showed that glycolysis and subsequent MG stress are triggered in PDAC cells rendered resistant to gemcitabine when compared with parental cells. In fact, acquired resistance, following short and long-term gemcitabine challenges, correlated with the upregulation of GLUT1, LDHA, GLO1, and the accumulation of MG protein adducts. We showed that MG-mediated activation of heat shock response is, at least in part, the molecular mechanism underlying survival in gemcitabine-treated PDAC cells. This novel adverse effect of gemcitabine, i.e., induction of MG stress and HSR activation, is efficiently reversed using potent MG scavengers such as metformin and aminoguanidine. We propose that the MG blockade could be exploited to resensitize resistant PDAC tumors and to improve patient outcomes using gemcitabine therapy.
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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 OpenQuestion graph.