Background
Methotrexate (MTX) is an antimetabolite that interferes with folic-acid cycle enzymes (primarily Dihydrofolate Reductase), inhibiting cell growth. Thus, MTX is used to treat various cancers and other autoimmune diseases. Folic-acid cycle enzymes and protein-transporters exhibit extensive polymorphisms that strongly impact individual patients’ ability to handle MTX, especially at high doses. To delineate the effects of these polymorphisms, appropriate genomic models are needed.
Aim (Phase I of Methotrexate in Seriously Sick Kids (MiSSK) Study):
Design and build different in-vitro models for human cancer cell-lines that express polymorphisms of folic-acid cycle enzymes, using CRISPR/Cas9 genomic engineering.
Methodology and results:
Cellular models were generated using polymorphisms with the most significant effect on MTX kinetics; methylene tetrahydrofolate reductase (MTHFR) enzyme and reduced-folate carrier (RFC/SLC19A1) transporter-protein. Human osteosarcoma cells (143B) and lymphoblastic-leukaemia cells (CCRF-CEM119) were used to quantify the effect in cancer cells whilst human embryonic-kidney cells (HEK293) were utilised as a non-cancer-control. Each cell-line underwent the following modifications:
After generation, the polymorphic-variant cell models were tested for MTX biological cytotoxic effects, using proliferation/viability assays (IncuCyteZOOM real-time cell monitoring). Metabolic effects were investigated by determining residual MTX concentrations in media and cell-lysates via a novel High-Performance Liquid Chromatography (HPLC) methodology.
Conclusion:
Polymorphic-variant cell models were successfully generated to examine the relationship between genomics and MTX metabolism in an attempt to individualise MTX treatment in practice.