The development of safe and effective therapies requires a deeper understanding of cancer cell biology. With effective cell analysis tools and validated experimental methods, Alfa Oncology provides pancreatic cancer (PC) cell metabolism research services to help reveal cancer cell biology as well as the tumor microenvironment from a metabolic perspective.
Unique metabolic features of PC
Pancreatic ductal adenocarcinoma (PDAC) is characterized by dense and fibrotic stroma and high interstitial pressure due to a prominent desmoplastic stromal reaction. Thus, PDAC tumor cells face hypoxia and nutrient deficiency. Several changes occur as a result of hypoxia: increased glycolysis and increased amino acid (AA) production from protein degradation and glycosylation as well as fatty acid synthesis. As a typical feature of PDAC and hypoxia is related to poor prognosis. Preclinical studies have demonstrated that hypoxia not only increases cancer cell proliferation, survival, epithelial-to-mesenchymal transition (EMT), invasiveness, and metastasis but also resistance to chemotherapy and radiotherapy. Despite facing hypoxia and nutritional deficiencies, PDAC cancer cells exhibit extraordinary growth advantages. They survive and thrive on three main types, including,
- PDAC cells exhibit complex and heterogeneous reprogramming of nutrient intracellular energy metabolism, including glucose, amino acid, and lipid metabolism
- Improving nutrient access to PDAC through scavenging and recycling has been shown to be applicable
- Performing metabolic crosstalk with stromal components within the microenvironment
Fig1. The landscape of metabolic pathways in pancreatic cancer cells. (Qin, C., et al., 2020)
The service offering at Alfa Oncology
Our cancer cell metabolism analysis platform relies on advanced technology and specialized personnel to measure cancer cell metabolism and function in real-time. Our service can quantify metabolic function under a variety of conditions to provide accurate physiologically relevant metabolic data, involving mitochondrial function, glycolytic function, metabolic phenotype, and cellular fuel preference. To explore metabolic changes and associated metabolic therapies by measuring bioenergetic metabolism and metabolic conversion of cancer cell proliferation effects to increase the understanding of PC. In addition, we can help detect the tumor microenvironment and help build better tumor models. Explore the metabolic phenotype of cancer cells under different substrate or culture conditions in 2D or 3D cell models and assess how substrate availability regulates metabolic homeostasis.
Benefits of our services:
-Efficient, simultaneous measurement of two metabolic pathways
Application of our services
Activation of KRAS mutations in PDAC is considered a major driver of carcinogenesis; however, to date, they have been shown to be poorer drug targets. Addressing downstream metabolic alterations to inhibit tumor growth in PDAC may be another useful attempt, including
- Blocking the glycolytic switch of cancer cells via glycolytic enzyme pyruvate kinase M2 (PKM2)
- Addressing glycolysis via lactate dehydrogenase-A (LDH-A)
- Blocking lactate transport and efflux
- Targeting glutamine metabolism
- Inducing asparagine deprivation with L-asparaginase
- Targeting lipid metabolism
- Inhibiting autophagy and macropinocytosis, such as hydroxychloroquine and mTOR inhibitors
- Metformin (non-specific OXPHOS inhibitor)
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- Qin, C., Yang, G., Yang, J., Ren, B., Wang, H., Chen, G., ... & Zhao, Y. (2020). Metabolism of pancreatic cancer: Paving the way to better anticancer strategies. Molecular cancer, 19(1), 1-19.
- Cohen, R., Neuzillet, C., Tijeras-Raballand, A., Faivre, S., de Gramont, A., & Raymond, E. (2015). Targeting cancer cell metabolism in pancreatic adenocarcinoma. Oncotarget, 6(19), 16832.
- Halbrook, C. J., & Lyssiotis, C. A. (2017). Employing metabolism to improve the diagnosis and treatment of pancreatic cancer. Cancer cell, 31(1), 5-19.