Metabolomics in Cancer Research

Metabolomics comprehensively characterizes small polar and lipid metabolites, yielding a snapshot of physiological processes that vary according to the pathological state of cells, tissues, and organs. Therefore, metabolomics profiling can help to identify specific metabolic changes in cancer cells and tissues, providing a deeper understanding of the role altered cellular metabolism plays in tumorigenesis, as well as in disease progression. Furthermore, targeting cancer metabolism pathways with metabolomics will be useful in determining critical biomarkers for early detection and therapeutic interventions.

Metabolomics brings us closer to the phenotype of an individual, providing a direct readout of metabolic changes that occur in the tumor microenvironment.

HMT’s metabolomics

HMT’s metabolome analysis employs CE-MS & LC-MS platforms. Our technologies are optimized to measure metabolites related to cellular energy metabolism, e.g., amino acids, short-chain fatty acids, polyamines, in most types of samples, including blood, tissues, and cultured cells.

Quantitation Quantitation
Over 100 polar metabolites involved in cancer metabolism are quantifiable with single- or multi-point calibration.
High resolution High resolution
Good separation of structural isomers, e.g. isobaric fatty acids, oxidative products.

Examples of samples that can be analyzed at HMT

Biofluids (plasma, serum, saliva, urine, etc.)

  • systemic “footprint” of tumor metabolism
  • discovery of biomarkers & diagnostic markers
  • monitor therapy-mediated changes
Cultured cells

  • assessment of novel therapeutics
  • determine drug sensitivity in cancer cells
  • identify metabolic changes in a time-dependent manner
Tissue extracts, biopsies, etc.

  • “snap-shot” of tumor metabolism
  • enhanced evaluation of disease progression
  • monitor therapy-mediated changes

Recent publications

1. N-acylsphingosine amidohydrolase 1 promotes melanoma growth and metastasis by suppressing peroxisome biogenesis-induced ROS production.
Malvi et al. Mol Metab. 2021. 101217
2. Metabolic compensation activates pro-survival mTORC1 signaling upon 3-phosphoglycerate dehydrogenase inhibition in osteosarcoma.
Rathore et al. Cell Rep. 2021. 34(4): 108678
3. Subpopulation targeting of pyruvate dehydrogenase and GLUT1 decouples metabolic heterogeneity during collective cancer cell invasion.
Commander et al. Nat Commun. 2020. 11(1):1533
4. Targeting pheochromocytoma/paraganglioma with polyamine inhibitors.
Rai et al. Metabolism. 2020. 110:154297
5. Genome-wide CRISPR/Cas9 library screening identified PHGDH as a critical driver for Sorafenib resistance in HCC.
Wei et al. Nat Commun. 2019. 10(1): 4681
6. Inducing cancer indolence by targeting mitochondrial Complex I is potentiated by blocking macrophage-mediated adaptive responses.
Kurelac et al. Nat Commun. 2019. 10(1): 903
7. Tumor metastasis to lymph nodes requires YAP-dependent metabolic adaptation.
Lee et al. Science. 2019. 363: 644-649
8. Dysregulated transmethylation leading to hepatocellular carcinoma compromises redox homeostasis and glucose formation.
Hughey et al. Mol Metab. 2019. 23: 1-13
9. Pyruvate secreted from patient-derived cancer-associated fibroblasts supports survival of primary lymphoma cells.
Sakamoto et al. Cancer Sci. 2019. 110(1): 269-278
10. Metabolic determinants of sensitivity to phosphatidylinositol 3-kinase pathway inhibitor in small-cell lung carcinoma.
Makinoshima et al. Cancer Res. 2018. 78(9): 2179-2190
11. ADHFE1 is a breast cancer oncogene and induces metabolic reprogramming.
Mishra et al. J Clin Invest. 2018. 128(1): 323-340
12. PKM1 confers metabolic advantages and promotes cell-autonomous tumor cell growth.
Morita et al. Cancer Cell. 2018. 33(3): 355-367


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