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Pancreatic Cancer Cell Metabolism Research
Safe and effective therapy development requires a deeper understanding of cancer cell biology. With effective cell analysis tools and validated experimental methods, Alfa Cytology provides pancreatic cancer (PC) cell metabolism research services to help reveal cancer cell biology and the tumor microenvironment from a metabolic perspective.
Unique Metabolic Features of Pancreatic Cancer
Pancreatic cancer is characterized by dense and fibrotic stroma and high interstitial pressure. Thus, pancreatic cancer cells face hypoxia and nutrient deficiency. Several changes occur in hypoxia, such as increased glycolysis and amino acid (AA) production from protein degradation or glycosylation and fatty acid synthesis. A typical feature of pancreatic cancer hypoxia is related to poor prognosis. Preclinical studies have demonstrated that hypoxia increases cancer cell proliferation, survival, epithelial-to-mesenchymal transition (EMT), invasiveness, metastasis, and resistance to chemotherapy or radiotherapy.
Fig. 1 Hypoxia and hypoxia-mediated metabolic abnormalities contribute to tumor immunosuppressive microenvironment. (Hao, X.; et al., 2021)
Pancreatic Cancer Cell Metabolic Pathways
Despite facing hypoxia and nutritional deficiencies, pancreatic cancer cells exhibit extraordinary growth advantages. They survive and thrive on three main types.
- Pancreatic cancer cells exhibit complex and heterogeneous reprogramming of nutrient intracellular energy metabolism, including glucose, amino acid, and lipid metabolism.
- Improving nutrient access to pancreatic cancer through scavenging and recycling is applicable.
- Performing metabolic crosstalk with stromal components within the microenvironment.
Fig. 2 The landscape of metabolic pathways in pancreatic cancer cells. (Qin, C.; et al., 2020)
Our Services
Our cancer cell metabolism analysis platform relies on advanced technology and specialized personnel to measure pancreatic 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, including but not limited to the following.
- Mitochondrial function
- Metabolic phenotype
- Glycolytic function
- Cellular fuel preference
In addition, we measure the effects of biological energy metabolism and metabolic transformation on cancer cell proliferation to explore metabolic changes and related metabolic therapies. 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.
Application of Our Services
Activation of KRAS mutations in pancreatic cancer is considered a major driver of carcinogenesis. However, there is still a great need for highly targeted drug development. Addressing downstream metabolic alterations to inhibit tumor growth in pancreatic cancer may be another useful attempt.
Blocking the glycolytic switch of cancer cells via glycolytic enzyme pyruvate kinase M2
Addressing glycolysis via lactate dehydrogenase-A
Inducing asparagine deprivation with L-asparaginase
Inhibiting autophagy and macrophages, such as mTOR inhibitors
Blocking lactate transport and efflux
Targeting glutamine metabolism
Targeting lipid metabolism
Non-specific OXPHOS inhibitor
Why Choose Us?
Scientific Experience
Professional team of scientists and more than ten years of experience in pancreatic cancer
Customized Service
Tailored services dedicated to ensuring customer satisfaction
Data Security
Strictly keep confidential the client's project information and experimental data
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References
- Hao, X., et al. Metabolic reprogramming due to hypoxia in pancreatic cancer: Implications for tumor formation, immunity, and more. Biomed Pharmacother. 2021 Sep;141:111798. doi: 10.1016/j.biopha.2021.111798
- Qin, C., et al. Metabolism of pancreatic cancer: paving the way to better anticancer strategies. Mol Cancer 2020, 19, 50. https://doi.org/10.1186/s12943-020-01169-7
