Pathological roles of c-Met in bladder cancer: Association with cyclooxygenase-2, heme oxygenase-1, vascular endothelial growth factor-A and programmed death ligand 1.
bladder cancer
c-Met
cyclooxygenase-2
heme oxygenase-1
phosphorylation
programmed death ligand 1
vascular endothelial growth factor-A
Journal
Oncology letters
ISSN: 1792-1074
Titre abrégé: Oncol Lett
Pays: Greece
ID NLM: 101531236
Informations de publication
Date de publication:
Jul 2020
Jul 2020
Historique:
received:
11
11
2019
accepted:
18
02
2020
entrez:
23
6
2020
pubmed:
23
6
2020
medline:
23
6
2020
Statut:
ppublish
Résumé
c-Met is a receptor tyrosine kinase that binds a specific ligand, namely hepatocyte growth factor (HGF). The HGF/c-Met system is important for malignant aggressiveness in various types of cancer, including bladder cancer (BC). However, although phosphorylation is the essential step required for biological activation of c-Met, pathological roles of phosphorylated c-Met at the clinical and molecular levels in patients with BC are not fully understood. In the present study, the expression levels of c-Met and the phosphorylation of two of its tyrosine residues (pY1234/pY1235 and pY1349) were immunohistochemically examined in 185 BC tissues. The associations between these expression levels and cancer cell invasion, metastasis, and cyclooxygenase-2 (COX-2), heme oxygenase-1 (HO-1), VEGF-A and programmed death ligand 1 (PD-L1) levels were investigated. c-Met was associated with muscle invasion (P=0.021), as well as the expression levels of HO-1 (P=0.028) and PD-L1 (P<0.001), whereas pY1349 c-Met was associated with muscle invasion (P=0.003), metastasis (P=0.025), and COX-2 (P=0.017), HO-1 (P=0.031) and PD-L1 (P=0.001) expression. By contrast, pY1234/1235 c-Met was associated with muscle invasion and metastasis (P=0.006 and P=0.012, respectively), but not with the panel of cancer-associated molecules. Furthermore, COX-2 and PD-L1 expression were associated with muscle invasion and metastasis, respectively (P=0.045 and P=0.036, respectively). Hence, c-Met serves important roles in muscle invasion by regulating HO-1 and PD-L1, whereas its phosphorylation at Y1349 is associated with muscle invasion and metastasis via the regulation of COX-2, HO-1 and PD-L1 in patients with BC. Furthermore, phosphorylation at Y1234/1235 may lead to muscle invasion and metastasis via alternate mechanisms associated with c-Met and pY1349 c-Met.
Identifiants
pubmed: 32565941
doi: 10.3892/ol.2020.11540
pii: OL-0-0-11540
pmc: PMC7285828
doi:
Types de publication
Journal Article
Langues
eng
Pagination
135-144Informations de copyright
Copyright: © Mukae et al.
Références
J Transl Med. 2017 Feb 23;15(1):46
pubmed: 28231855
Hum Pathol. 2018 Nov;81:184-191
pubmed: 29969606
Vet Comp Oncol. 2019 Jun;17(2):194-207
pubmed: 30767381
Biochem Biophys Res Commun. 2003 Mar 21;302(4):892-7
pubmed: 12646256
Elife. 2016 Mar 17;5:
pubmed: 26987019
Int J Clin Exp Pathol. 2015 Apr 01;8(4):3719-26
pubmed: 26097553
Oncol Lett. 2017 Jan;13(1):275-280
pubmed: 28123555
Hum Pathol. 2009 Apr;40(4):496-504
pubmed: 19121849
J Clin Oncol. 2000 Sep;18(17):3068-77
pubmed: 11001674
Nat Rev Mol Cell Biol. 2003 Dec;4(12):915-25
pubmed: 14685170
Oncol Lett. 2019 Jun;17(6):5487-5498
pubmed: 31186768
Onco Targets Ther. 2019 Apr 10;12:2695-2702
pubmed: 31114223
Food Chem Toxicol. 2017 Nov;109(Pt 1):143-154
pubmed: 28870684
Oncotarget. 2017 Aug 3;8(40):66849-66864
pubmed: 28978000
PLoS One. 2017 Apr 13;12(4):e0175494
pubmed: 28406993
Int J Clin Exp Pathol. 2015 Feb 01;8(2):1776-82
pubmed: 25973067
In Vitro Cell Dev Biol Anim. 2017 Mar;53(3):272-276
pubmed: 27752923
Clin Cancer Res. 2012 Apr 15;18(8):2269-77
pubmed: 22374333
Cell Commun Signal. 2017 Feb 17;15(1):10
pubmed: 28212658
Hum Pathol. 2014 Sep;45(9):1830-8
pubmed: 24957789
Cancer Manag Res. 2019 May 08;11:4171-4184
pubmed: 31190987
Cancers (Basel). 2017 Dec 12;9(12):
pubmed: 29231907
Expert Opin Investig Drugs. 2015;24(7):913-27
pubmed: 26098435
J Biol Chem. 2015 Mar 27;290(13):8110-20
pubmed: 25645920
Cancer. 2001 Jul 1;92(1):188-93
pubmed: 11443626
Int J Mol Sci. 2018 Nov 22;19(12):
pubmed: 30469509
Target Oncol. 2017 Aug;12(4):487-494
pubmed: 28550387
Trends Biochem Sci. 2003 Oct;28(10):527-33
pubmed: 14559181
Oral Dis. 2020 Apr;26(3):511-526
pubmed: 30866171
Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):800-6
pubmed: 16467091
Transl Res. 2016 Sep;175:116-28
pubmed: 27140699
J Urol. 2005 Jan;173(1):56-60
pubmed: 15592025
Urol Oncol. 2017 May;35(5):257-263
pubmed: 28291636
Front Immunol. 2017 Dec 04;8:1597
pubmed: 29255458
Cancers (Basel). 2014 Dec 16;6(4):2387-403
pubmed: 25521854
BMC Cancer. 2016 May 19;16:321
pubmed: 27198692
Adv Exp Med Biol. 2014;816:183-96
pubmed: 24818724
Int J Mol Sci. 2018 Nov 14;19(11):
pubmed: 30441809
Clin Cancer Res. 2006 Aug 15;12(16):4876-81
pubmed: 16914575
Virchows Arch. 2019 Nov;475(5):599-608
pubmed: 31267201
Int J Mol Sci. 2018 Oct 24;19(11):
pubmed: 30352967
J Biol Chem. 1991 Oct 15;266(29):19558-64
pubmed: 1655790
Jpn J Clin Oncol. 2018 Oct 1;48(10):934-941
pubmed: 30169681
Cancer Treat Rev. 2017 Mar;54:58-67
pubmed: 28214651
Urology. 2019 Sep;131:150-156
pubmed: 31201825