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    Association of transcriptional levels of folate-mediated one-carbon metabolism-related Ferrostatin 1 in cancer cell lines with drug treatment response
    Dong-Joon Min1, Suleyman Vural1, Julia Krushkal∗ Computational and Systems Biology Branch, Biometric Research Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, 9609 Medical Center Dr., Rockville, MD 20850, United States
    Folate-mediated one-carbon metabolism is essential for growth and survival of cancer cells. We investigated whether the response of cancer cells to antitumor treatment may be partially in-fluenced by variation in expression of one-carbon metabolism genes. We used cancer cell line in-formation from the Cancer Cell Line Encyclopedia and the Genomics of Drug Sensitivity in Cancer resources to examine whether variation in pretreatment expression of one-carbon metabolism-related genes was associated with response to treatment. GART, TYMS, SHMT2, MTR, ALDH2, BHMT, MAT2B, MTHFD2, NNMT, and SLC46A1 showed modest statistically significant correla-tions with response to a variety of antitumor agents. Higher expression levels of SLC46A1 were associated with resistance to multiple agents, whereas elevated expression of GART, TYMS, SHMT2, MTR, BHMT, and MAT2B was associated with chemosensitivity to multiple drugs. NNMT expression was bimodally distributed and showed different directions of association with various agents. Correlation of increased NNMT expression with sensitivity to dasatinib was validated in
    Abbreviations: 10-formylTHF, 10-formyltetrahydrofolate; 5,10-methylene-THF, 5,10-methylenethetrahydrofolate; AHCY, adenosylhomocys-teinase; ALDH1L1, aldehyde dehydrogenase 1 family, member L1; ALDH2, aldehyde dehydrogenase 2 family; ALK, anaplastic lymphoma kinase; ALL, acute lymphoblastic leukemia; AMT, aminomethyltransferase; ATF4, activating transcription factor 4; ATIC, 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase; BHMT, betaine-homocysteine methyltransferase; CBS, cystathionine β-synthase; CCLE, Cancer Cell Line Encyclopedia; CTH, cystathionase; DDR1, discoidin domain receptor 1; DHF, dihydrofolate; DHFR, di-hydrofolate reductase; EDNRA, endothelin-1 receptor (endothelin receptor type A); EGFR, epidermal growth factor receptor; FDR, false discovery rate; FOLH1, folate hydrolase 1; FOLR1, folate receptor 1; FOLR2, folate receptor 2; FOLR3, folate receptor 3; FTCD, formimi-doyltransferase cyclodeaminase; GART, glycinamide ribonucleotide formyltransferase; GDSC, Genomics of Drug Sensitivity in Cancer; HDAC, histone deacetylase; HIF-1, hypoxia-inducible factor 1; LXR, liver X receptor; MAT1A, L-methionine S-adenosyltransferase 1, alpha; MAT2A, L-methionine S-adenosyltransferase 2, alpha; MAT2B, L-methionine S-adenosyltransferase 2, beta; MTHFD1, methylenetetrahydrofolate de-hydrogenase 1; MTHFD2, methylenetetrahydrofolate dehydrogenase 2; MTHFD2L, methylenetetrahydrofolate dehydrogenase 2-like; MTHFR, 5, 10-methylenetetrahydrafolate reductase; MTHFS, methylenetetrahydrofolate synthase; mTOR, mammalian target of rapamycin; MTR, me-thionine synthase; MTRR, 5-methyltetrahydrafolate-homocysteine methyltransferase reductase; NCI, National Cancer Institute; NNMT, nicoti-namide N-methyltransferase; OCM, one-carbon metabolism; OXPHOS, oxidative phosphorylation; PDK, pyruvate dehydrogenase kinase; PEMT, phosphatidylethanolamine-N-methyltransferase; PHGDH, phosphoglycerate dehydrogenase; PLK3, polo-like kinase 3; RIPK1, receptor-interacting serine/threonine-protein kinase 1; RMA, Robust Multiarray Average; ROS, reactive oxygen species; SAH, S-adenosylhomocysteine; SAM, S-adenosylmethionine; SHMT1, serine hydroxymethyl transferase 1; SHMT2, serine hydroxymethyl transferase 2; SLC19A1, solute car-rier family 19 member 1; SLC46A1, solute carrier family 46 member 1; TCA, tricarboxylic acid; TCN2, transcobalamin 2; THF, tetrahydrofolate; TYMS, thymidylate synthase; VEGFR, vascular endothelial growth factor receptor.