Overexpression of hydroxyproline via EGLN/HIF1A is associated with distant metastasis in pancreatic cancer.
EGLN
HIF1A
distant metastasis
hydroxyproline
pancreatic cancer
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
2020
Historique:
received:
07
11
2019
accepted:
10
01
2020
entrez:
9
9
2020
pubmed:
10
9
2020
medline:
10
9
2020
Statut:
epublish
Résumé
For pancreatic cancer, the probability of distant metastasis can help choose the best course of treatment. The aim of this study is to establish the efficacy of hydroxyproline as a biomarker for distant metastasis for pancreatic cancer and to clarify the mechanism of EGLN/HIF1A axis that controls the invasion and metastasis. Metabolites (hydroxyproline) and genes (EGLN2 and EGLN3) were identified by metabolome analysis of the serum with pancreatic cancers with and without distant metastasis. The mechanism of EGLN/HIF1A axis including angiogenesis was examined in pancreatic cancer cells. Hydroxyproline associated with these mechanisms was evaluated to suggest the association with overall survival in pancreatic cancer. Decreased expression of EGLN2 and EGLN3 in pancreatic cancer, via the HIF1A and TGF ß1 pathway, was associated with the induction of angiogenic factors, increased vascular invasion, and poor overall patient survival. Hydroxyproline concentrations were regulated via the HIF1A pathway by EGLN2 and EGLN3, and that increased concentrations of hydroxyproline promote the invasion and metastasis of pancreatic cancer cells. These results suggested that the expression of hydroxyproline through the HIF1A pathway induced by EGLN2 and EGLN3 could be a surrogate marker for treatment and might predict distant metastasis in pancreatic cancer.
Types de publication
Journal Article
Langues
eng
Pagination
2570-2581Informations de copyright
AJCR Copyright © 2020.
Déclaration de conflit d'intérêts
None.
Références
Cancer Res. 2003 Dec 15;63(24):8777-83
pubmed: 14695194
Science. 2009 Jun 12;324(5933):1457-61
pubmed: 19460966
Anticancer Res. 2010 Mar;30(3):1007-14
pubmed: 20393028
Int J Mol Sci. 2017 Apr 04;18(4):
pubmed: 28375170
Cancer Genet. 2014 May;207(5):188-94
pubmed: 24935227
Proc Natl Acad Sci U S A. 2012 Feb 21;109(8):2760-5
pubmed: 21930940
J Gastrointest Surg. 2015 Mar;19(3):438-44
pubmed: 25567663
Br J Cancer. 2010 Nov 9;103(10):1571-9
pubmed: 20978507
Oncogene. 2010 Feb 4;29(5):625-34
pubmed: 19946328
CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29
pubmed: 24399786
J Surg Oncol. 2016 Sep;114(3):336-41
pubmed: 27501338
Lancet. 2016 Jul 2;388(10039):73-85
pubmed: 26830752
Mol Cell. 2008 May 23;30(4):393-402
pubmed: 18498744
Cancer Res. 2011 Jun 1;71(11):4015-27
pubmed: 21512133
Clin Cancer Res. 2018 Jan 15;24(2):474-485
pubmed: 29084919
Proc Natl Acad Sci U S A. 2010 Jan 19;107(3):1100-5
pubmed: 20080567
J Am Coll Surg. 2014 Mar;218(3):401-11
pubmed: 24484730
Br J Cancer. 2016 Mar 29;114(7):737-43
pubmed: 27022826
Annu Rev Biochem. 1980;49:1005-61
pubmed: 6250440
Cell Death Dis. 2018 Feb 23;9(3):321
pubmed: 29476053
J Gastroenterol Hepatol. 2005 Jul;20(7):1109-14
pubmed: 15955222