A High-Resolution Mass Spectrometry-Based Quantitative Metabolomic Workflow Highlights Defects in 5-Fluorouracil Metabolism in Cancer Cells with Acquired Chemoresistance.
5-Fluorouracil
chemoresistance
colorectal cancer
high-resolution mass spectrometry
metabolites
nucleotide analogue
precursor isotopes
single ion monitoring
Journal
Biology
ISSN: 2079-7737
Titre abrégé: Biology (Basel)
Pays: Switzerland
ID NLM: 101587988
Informations de publication
Date de publication:
06 May 2020
06 May 2020
Historique:
received:
03
03
2020
revised:
20
04
2020
accepted:
21
04
2020
entrez:
10
5
2020
pubmed:
10
5
2020
medline:
10
5
2020
Statut:
epublish
Résumé
Currently, 5-fluorouracil (5-FU)-based combination chemotherapy is the mainstay in the treatment of metastatic colorectal cancer (CRC), which benefits approximately 50% of the patients. However, these tumors inevitably acquire chemoresistance resulting in treatment failure. The molecular mechanisms driving acquired chemotherapeutic drug resistance in CRC is fundamental for the development of novel strategies for circumventing resistance. However, the specific phenomenon that drives the cancer cells to acquire resistance is poorly understood. Understanding the molecular mechanisms that regulate chemoresistance will uncover new avenues for the treatment of CRC. Among the various mechanisms of acquired chemoresistance, defects in the drug metabolism pathways could play a major role. In the case of 5-FU, it gets converted into various active metabolites, which, directly or indirectly, interferes with the replication and transcription of dividing cells causing DNA and RNA damage. In this project, we developed a high-resolution mass spectrometry-based method to effectively extract and quantify levels of the 5-FU metabolites in cell lysates and media of parental and 5-FU resistant LIM1215 CRC cells. The analysis highlighted that the levels of 5-FU metabolites are significantly reduced in 5-FU resistant cells. Specifically, the level of the nucleotide fluorodeoxyuridine monophosphate (FdUMP) is reduced with treatment of 5-FU clarifying the compromised 5-FU metabolism in resistant cells. Corroborating the metabolomic analysis, treatment of the resistant cells with FdUMP, an active metabolite of 5-FU, resulted in effective killing of the resistant cells. Overall, in this study, an effective protocol was developed for comparative quantitation of polar metabolites and nucleotide analogues from the adherent cells efficiently. Furthermore, the utility of FdUMP as an alternative for CRC therapy is highlighted.
Identifiants
pubmed: 32384705
pii: biology9050096
doi: 10.3390/biology9050096
pmc: PMC7284906
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
Proc Natl Acad Sci U S A. 2019 Jul 30;116(31):15469-15474
pubmed: 31311867
Molecules. 2008 Aug 05;13(8):1551-69
pubmed: 18794772
J Chromatogr B Analyt Technol Biomed Life Sci. 2009 Oct 1;877(27):2937-44
pubmed: 19620028
BMC Bioinformatics. 2012;13 Suppl 16:S9
pubmed: 23176545
Nat Methods. 2019 Apr;16(4):299-302
pubmed: 30886413
J Proteome Res. 2011 Apr 1;10(4):2104-12
pubmed: 21322650
J Food Drug Anal. 2016 Jan;24(1):56-62
pubmed: 28911409
Gigascience. 2017 Jul 1;6(7):1-20
pubmed: 28520864
Oncol Rep. 2008 Jul;20(1):89-98
pubmed: 18575723
Sci Rep. 2013;3:2495
pubmed: 23970067
Nat Rev Cancer. 2003 Jul;3(7):502-16
pubmed: 12835670
Metabolites. 2013 Jun 13;3(2):506-16
pubmed: 24958003
J Pharm Biomed Anal. 2015 Jun 10;110:58-66
pubmed: 25804433
Ann Oncol. 2009 May;20 Suppl 4:49-50
pubmed: 19454461
Metabolomics. 2017;13(7):79
pubmed: 28596718
Sci Data. 2019 Aug 2;6(1):141
pubmed: 31375670
Sci Rep. 2019 Jan 17;9(1):195
pubmed: 30655588
CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49
pubmed: 19474385
Clin Cancer Res. 1999 Mar;5(3):643-54
pubmed: 10100718
Lancet. 2005 Jan 8-14;365(9454):153-65
pubmed: 15639298
Nucleic Acids Res. 2016 Jan 4;44(D1):D969-74
pubmed: 26496946
Rapid Commun Mass Spectrom. 2016 Jul 15;30(13):1560-6
pubmed: 27321843
Talanta. 2014 Feb;119:178-80
pubmed: 24401401
Rapid Commun Mass Spectrom. 2008;22(2):224-30
pubmed: 18085512
Cancer Invest. 2006 Apr-May;24(3):235-41
pubmed: 16809149
Nat Biotechnol. 2016 Nov 8;34(11):1099-1101
pubmed: 27824832
Chin Med. 2010 Jul 25;5:26
pubmed: 20653978
Analyst. 2019 Jan 28;144(3):782-793
pubmed: 30426983
Nucleic Acids Res. 2018 Jan 4;46(D1):D608-D617
pubmed: 29140435
J Am Soc Mass Spectrom. 2017 Nov;28(11):2280-2287
pubmed: 28721670
Eur J Cancer. 2002 May;38(7):1000-15
pubmed: 11978525
Talanta. 2017 May 1;166:249-254
pubmed: 28213230
Int J Oncol. 2002 Aug;21(2):303-8
pubmed: 12118325
Sci Rep. 2018 Feb 22;8(1):3446
pubmed: 29472576
Br J Clin Pharmacol. 2016 May;81(5):949-57
pubmed: 26718616
Crit Rev Oncol Hematol. 2010 May;74(2):106-33
pubmed: 20138539
Anal Chem. 2016 Aug 2;88(15):7556-66
pubmed: 27398867
Metabolomics. 2014 Apr 4;10(2):312-323
pubmed: 25411574
Nat Rev Cancer. 2003 May;3(5):330-8
pubmed: 12724731
Mol Cell Proteomics. 2012 Dec;11(12):1709-23
pubmed: 22962056
Bioinformatics. 2009 Jan 15;25(2):218-24
pubmed: 19015140
Bioinformatics. 2010 Apr 1;26(7):966-8
pubmed: 20147306
Mol Cancer Ther. 2007 Jan;6(1):122-7
pubmed: 17237272
Anal Chim Acta. 2013 May 30;780:65-73
pubmed: 23680552
Proteomics. 2014 Feb;14(2-3):169-80
pubmed: 24307133
Clin Biochem. 2005 Apr;38(4):310-8
pubmed: 15766732
Bioinformatics. 2008 Aug 15;24(16):i49-i55
pubmed: 18689839
Expert Rev Proteomics. 2016 Dec;13(12):1063-1071
pubmed: 27798968
Mol Cancer Ther. 2008 Sep;7(9):3029-37
pubmed: 18790783
J Am Soc Mass Spectrom. 2017 Nov;28(11):2384-2392
pubmed: 28733968
J Agric Food Chem. 2007 Feb 7;55(3):551-60
pubmed: 17263440