ArticlePancreas2012
Inhibition of glycogen phosphorylation induces changes in cellular proteome and signaling pathways in MIA pancreatic cancer cells.
Article in Pancreas, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Metabolic buffering restricts phenotype switching in melanoma.The EMBO journal · 2026Article
- Deciphering Cancer Complexity: Integrative Proteogenomics and Proteomics Approaches for Biomarker Discovery.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Cellular hierarchy framework based on single-cell/multi-patient sample sequencing reveals metabolic biomarker PYGL as a therapeutic target for HNSCC.Journal of experimental & clinical cancer research : CR · 2023Article
- New thoughts and findings on invasion and metastasis of pancreatic ductal adenocarcinoma (PDAC) from comparative proteomics: multi-target therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- PYGL-mediated glucose metabolism reprogramming promotes EMT phenotype and metastasis of pancreatic cancer.International journal of biological sciences · 2023Article
- Metabolic alterations and mitochondrial dysfunction underlie hepatocellular carcinoma cell death induced by a glycogen metabolic inhibitor.Biochemical pharmacology · 2022Article
- The Molecular Floodgates of Stress-Induced Senescence Reveal Translation, Signalling and Protein Activity Central to the Post-Mortem Proteome.International journal of molecular sciences · 2020Article
- Revisiting Glycogen in Cancer: A Conspicuous and Targetable Enabler of Malignant Transformation.Frontiers in oncology · 2020Review
- A critical review of the role of MBiochimica et biophysica acta. Reviews on cancer · 2019Review
- The Warburg effect: a balance of flux analysis.Metabolomics : Official journal of the Metabolomic Society · 2015Article
- Targeting glycogen metabolism in bladder cancer.Nature reviews. Urology · 2015Review
- Xanthohumol-Mediated Suppression of Notch1 Signaling Is Associated with Antitumor Activity in Human Pancreatic Cancer Cells.Molecular cancer therapeutics · 2015Article
- Metabolic Consequences of LDHA inhibition by Epigallocatechin Gallate and Oxamate in MIA PaCa-2 Pancreatic Cancer Cells.Metabolomics : Official journal of the Metabolomic Society · 2015Article
- Role of the tumor suppressor IQGAP2 in metabolic homeostasis: Possible link between diabetes and cancer.Metabolomics : Official journal of the Metabolomic Society · 2014Article
- Requirement of glycogenolysis for uptake of increased extracellular K+ in astrocytes: potential implications for K+ homeostasis and glycogen usage in brain.Neurochemical research · 2013Article
- Prediction of functional phosphorylation sites by incorporating evolutionary information.Protein & cell · 2012Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
objectivesNovel quantitative proteomic approaches were used to study the effects of inhibition of glycogen phosphorylase on proteome and signaling pathways in MIA PaCa-2 pancreatic cancer cells.
methodsWe performed quantitative proteomic analysis in MIA PaCa-2 cancer cells treated with a stratified dose of CP-320626 (5-chloro-1H-indole-2-carboxylic acid [1-(4-fuorobenzyl)-2-(4-hydroxypiperidin-1-yl)-2 oxoethyl] amide) (25, 50, and 100 μM). The effect of metabolic inhibition on cellular protein turnover dynamics was also studied using the modified SILAC (stable isotope labeling with amino acids in cell culture) method.
resultsA total of 22 protein spots and 4 phosphoprotein spots were quantitatively analyzed. We found that dynamic expression of total proteins and phosphoproteins was significantly changed in MIA PaCa-2 cells treated with an incremental dose of CP-320626. Functional analyses suggested that most of the proteins differentially expressed were in the pathways of mitogen-activated protein kinase/extracellular signal-regulated kinase and tumor necrosis factor α/nuclear factor κB.
conclusionsSignaling pathways and metabolic pathways share many common cofactors and substrates forming an extended metabolic network. The restriction of substrate through 1 pathway such as inhibition of glycogen phosphorylation induces pervasive metabolomic and proteomic changes manifested in protein synthesis, breakdown, and posttranslational modification of signaling molecules. Our results suggest that quantitative proteomic is an important approach to understand the interaction between metabolism and signaling pathways.
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