Comparison of the amino acid profile between the nontumor and tumor regions in patients with lung cancer.

NSCLS amino acids energy metabolism gluconeogenesis tumor region

Journal

American journal of cancer research
ISSN: 2156-6976
Titre abrégé: Am J Cancer Res
Pays: United States
ID NLM: 101549944

Informations de publication

Date de publication:
2020
Historique:
received: 19 06 2020
accepted: 27 06 2020
entrez: 11 8 2020
pubmed: 11 8 2020
medline: 11 8 2020
Statut: epublish

Résumé

Energy metabolism in cancer cells is reprogrammed to meet the energy demands for cell proliferation under strict environments. In addition to the specifically activated metabolism of cancer, including the Warburg effect and glutaminolysis, most amino acids (AAs) are utilized for gluconeogenesis. Significant increases in AAs and energy metabolites in the tumor region occur in gastric and colon cancers. However, a different AA-related energy metabolism may exist in lung cancer because of the abundant blood supply to lung tissue. This study compared the profiles of AAs and their related metabolites in energy metabolism, analyzed by an HPLC-MS/MS system, between tissues from nontumor and tumor regions collected from 14 patients with non-small cell lung cancer (NSCLC). In the energic metabolism precursor categories, the glucogenic AAs, which included the pyruvate precursors (Ser, Gly, Thr, Ala, and Trp), the α-ketoglutarate precursors (Glu, Gln, and Pro) and the succinyl-CoA precursors (Val, Ile, and Met) were significantly increased in the tumor region compared to in the nontumor region. However, no significant differences existed between the two regions in the ketogenic AAs (Leu, Lys, and Tyr). These differences were not observed between the subgroups with and without diabetes mellitus in the two regions. The metabolites on the left-hand side of the TCA cycle were significantly higher in the tumor region, but no differences in metabolites in the right-hand side. The mRNA expressions of major AA transporters and cancer proliferation factors were also significantly increased in the tumor region, compared to these in their counterparts. In lung cancer, glucogenic AAs that are actively transported from circulating fluids would be predominantly utilized for gluconeogenesis, with and without diabetes mellitus. The characteristics of the AA-related metabolism would be associated with tissue-specific cell proliferation in patients with NSCLC.

Identifiants

pubmed: 32775007
pmc: PMC7407354

Types de publication

Journal Article

Langues

eng

Pagination

2145-2159

Informations de copyright

AJCR Copyright © 2020.

Déclaration de conflit d'intérêts

None.

Références

Cell Cycle. 2010 Oct 1;9(19):3884-6
pubmed: 20948290
Mol Cell. 2015 Nov 19;60(4):509-11
pubmed: 26590709
Endocr Relat Cancer. 2009 Dec;16(4):1103-23
pubmed: 19620249
J Thorac Oncol. 2016 Apr;11(4):516-23
pubmed: 26949046
Nat Clin Pract Endocrinol Metab. 2009 Jan;5(1):24-5
pubmed: 18981990
Mol Cell Biol. 1999 May;19(5):3278-88
pubmed: 10207053
Oncogene. 2015 Feb 19;34(8):1044-50
pubmed: 24632615
Nat Rev Cancer. 2016 Oct;16(10):619-34
pubmed: 27492215
Proc Natl Acad Sci U S A. 2014 Oct 21;111(42):E4394
pubmed: 25261555
Trends Biochem Sci. 1999 Feb;24(2):68-72
pubmed: 10098401
Anticancer Res. 1995 Mar-Apr;15(2):507-10
pubmed: 7763031
Science. 1956 Feb 24;123(3191):309-14
pubmed: 13298683
Oncogene. 2016 Jun 16;35(24):3201-8
pubmed: 26455325
JIMD Rep. 2019;43:53-61
pubmed: 29654547
BMC Cancer. 2010 Dec 22;10:690
pubmed: 21176209
PLoS One. 2011;6(9):e24143
pubmed: 21915291
Trends Biochem Sci. 2018 Oct;43(10):752-789
pubmed: 30177408
Exp Clin Endocrinol Diabetes. 2016 May;124(5):263-75
pubmed: 27219686
Am J Roentgenol Radium Ther Nucl Med. 1967 Jul;100(3):603-19
pubmed: 5230250
EMBO J. 2017 May 15;36(10):1302-1315
pubmed: 28420743
J Nucl Med. 1999 Apr;40(4):556-65
pubmed: 10210213
Mol Metab. 2020 Mar;33:48-66
pubmed: 31395464
J Biol Chem. 2011 Sep 9;286(36):31830-8
pubmed: 21771784
Springerplus. 2015 Sep 15;4:494
pubmed: 26389019
J Biomed Biotechnol. 2010;2010:427694
pubmed: 20454640
Cancer Res. 2009 Jun 1;69(11):4918-25
pubmed: 19458066
Anticancer Res. 2003 Mar-Apr;23(2A):1149-54
pubmed: 12820363
Mol Cell. 2015 Oct 15;60(2):195-207
pubmed: 26474064
Rapid Commun Mass Spectrom. 2009 May;23(10):1483-92
pubmed: 19350529
J Clin Invest. 2015 Feb;125(2):687-98
pubmed: 25607840
Mol Cancer. 2009 Jun 26;8:41
pubmed: 19558692
Int J Clin Oncol. 2014 Apr;19(2):364-72
pubmed: 23700142
Proc Natl Acad Sci U S A. 2014 Jul 22;111(29):10684-9
pubmed: 25009184
Mol Genet Metab. 2017 Mar;120(3):207-212
pubmed: 28041819

Auteurs

Haruka Namikawa-Kanai (H)

Department of Surgery, Tokyo Medical University Tokyo, Japan.
Department of Thoracic Surgery, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Teruo Miyazaki (T)

Joint Research Center, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Taisuke Matsubara (T)

Department of Surgery, Tokyo Medical University Tokyo, Japan.

Shunsuke Shigefuku (S)

Department of Surgery, Tokyo Medical University Tokyo, Japan.

Shotaro Ono (S)

Department of Thoracic Surgery, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Eiji Nakajima (E)

Department of Thoracic Surgery, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Yukio Morishita (Y)

Diagnostic Pathology Division, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Akira Honda (A)

Joint Research Center, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.
Department of Internal Medicine, Division of Gastroenterology and Hepatology, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Kinya Furukawa (K)

Department of Thoracic Surgery, Tokyo Medical University Ibaraki Medical Center Ibaraki, Japan.

Norihiko Ikeda (N)

Department of Surgery, Tokyo Medical University Tokyo, Japan.

Classifications MeSH