Altered glucose metabolism and proteolysis in pancreatic cancer cell conditioned myoblasts: searching for a gene expression pattern with a microarray analysis of 5000 skeletal muscle genes
- D Basso 1, C Millino , E Greco , C Romualdi , P Fogar , A Valerio , M Bellin , C-F Zambon , F Navaglia , N Dussini , A Avogaro , S Pedrazzoli , G Lanfranchi , M Plebani
- 1Department of Laboratory Medicine, University of Padova, Italy.
- 0Department of Laboratory Medicine, University of Padova, Italy.
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View abstract on PubMed
Summary
This summary is machine-generated.Pancreatic cancer cell conditioned media increased lactate production and induced proteolysis in myoblasts. This suggests significant alterations in gene expression, impacting glucose metabolism and cellular processes.
Area Of Science
- Biochemistry
- Molecular Biology
- Cell Biology
Background
- Pancreatic cancer is a complex disease with significant impact on host metabolism.
- Understanding the molecular crosstalk between cancer cells and host tissues is crucial for therapeutic development.
Purpose Of The Study
- To investigate the effects of pancreatic cancer cell conditioned media (CM) on mouse myoblast glucose metabolism and gene expression.
- To identify specific molecular pathways altered by pancreatic cancer CM.
Main Methods
- Incubation of mouse myoblasts with CM from various pancreatic cancer cell lines (MIAPaCa2, CAPAN-1, PANC-1, BxPC3) for 24 and 48 hours.
- Analysis of glucose metabolism by measuring lactate production.
- Gene expression profiling using a skeletal muscle cDNA microarray (5000 genes).
Main Results
- Pancreatic cancer CM significantly increased lactate production in myoblasts.
- No significant changes were observed in key glycolysis genes.
- Overexpression of genes involved in the tricarboxylic acid cycle (e.g., Propionyl Coenzyme A Carboxylase, Isocitrate Dehydrogenase 3 Beta) and intracellular signaling (PAFAH1B1, BCL-2).
- Underexpression of genes related to vesicle transport (IGFIIR, VAMP5) and muscle structural proteins (Sorcin, Actin Alpha, Troponin T1, Filamin A).
- Increased tyrosine accumulation indicated that proteolysis exceeded protein synthesis.
Conclusions
- Pancreatic cancer CM enhances lactate production and induces proteolysis in myoblasts.
- These effects are mediated by significant alterations in gene expression across multiple cellular pathways, including the tricarboxylic acid cycle and vesicle transport.
- The study highlights a complex molecular interaction between pancreatic cancer cells and skeletal muscle, potentially contributing to cancer cachexia.
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