NDRG1 suppresses vasculogenic mimicry and tumor aggressiveness in gastric carcinoma.

N-myc downstream regulated gene 1 epithelial-mesenchymal transition gastric carcinoma human epidermal growth factor receptor 2 vasculogenic mimicry

Journal

Oncology letters
ISSN: 1792-1074
Titre abrégé: Oncol Lett
Pays: Greece
ID NLM: 101531236

Informations de publication

Date de publication:
Sep 2019
Historique:
received: 06 09 2018
accepted: 24 06 2019
entrez: 28 8 2019
pubmed: 28 8 2019
medline: 28 8 2019
Statut: ppublish

Résumé

N-myc downstream regulated gene 1 (NDRG1) has been well characterized as a suppressor of metastasis in numerous types of carcinoma. NDRG1 inhibits the metastatic progression of cancer cells via its inhibitory effects on a wide variety of cellular signaling pathways. Vasculogenic mimicry (VM) refers to the unique ability of aggressive tumor cells to mimic the pattern of embryonic vasculogenic networks, and is the main reason for the poor prognosis and failure of antivascular therapy in gastric carcinoma (GC). Tumor cells can mimic the function of endothelial cells to exhibit VM through epithelial-mesenchymal transition (EMT). However, the potential function of NDRG1 in metastatic GC progression in patients has not yet been fully elucidated. To date, data regarding the function of NDRG1 in VM formation in GC have not been reported. The aim of the present study was to elucidate these unknown areas. To this end, 228 samples of human GC were used to identify the protein expression levels of NDRG1, VM-associated proteins and EMT-associated proteins via immunohistochemistry, and their clinical significance was assessed. In addition, the data of 415 patients with GC were collected from The Cancer Genome Atlas database. A functional enrichment analysis concerning NDRG1 was performed using Metascape and the Gene Set Enrichment Analysis (GSEA). In conclusion, the results of the present study indicate that NDRG1 is negatively correlated with poor prognosis through suppression of VM formation in GC. The results of the present study demonstrated that NDRG1 decreases EMT-associated protein expression and that HER2 expression may serve a significant role in this process. The Metascape and GSEA results also indirectly support this conclusion. The present study discusses the status NDRG1 as a prognostic and selective biomarker in GC, as well as current and future NDRG1-targeted therapies.

Identifiants

pubmed: 31452779
doi: 10.3892/ol.2019.10642
pii: OL-0-0-10642
pmc: PMC6704281
doi:

Types de publication

Journal Article

Langues

eng

Pagination

3003-3016

Références

Am J Pathol. 1999 Sep;155(3):739-52
pubmed: 10487832
Nature. 2000 Aug 3;406(6795):536-40
pubmed: 10952317
Proc Natl Acad Sci U S A. 2001 Jul 3;98(14):8018-23
pubmed: 11416160
Ann Oncol. 2004 Nov;15(11):1585-95
pubmed: 15520058
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108
pubmed: 15761078
Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50
pubmed: 16199517
Clin J Oncol Nurs. 2006 Apr;10(2):153-4
pubmed: 16708697
Exp Biol Med (Maywood). 2007 Nov;232(10):1300-7
pubmed: 17959842
Lancet Oncol. 2008 Mar;9(3):279-87
pubmed: 18308253
BMC Bioinformatics. 2008 Dec 29;9:559
pubmed: 19114008
Med Hypotheses. 2010 Feb;74(2):360-1
pubmed: 19744799
Hepatology. 2010 Feb;51(2):545-56
pubmed: 19957372
Breast Cancer Res Treat. 2011 Feb;126(1):1-14
pubmed: 20369286
Virchows Arch. 2010 Sep;457(3):299-307
pubmed: 20665045
Hepatology. 2011 Nov;54(5):1690-706
pubmed: 21748764
Cancer Lett. 2011 Nov 1;310(1):35-45
pubmed: 21763068
Arch Med Sci. 2011 Apr;7(2):287-93
pubmed: 22291769
Oncogene. 2013 Jan 31;32(5):544-53
pubmed: 22469978
PLoS One. 2012;7(7):e41312
pubmed: 22844455
J Cell Mol Med. 2013 Jan;17(1):116-22
pubmed: 23279650
Crit Rev Oncog. 2013;18(5):409-34
pubmed: 23879587
Gynecol Oncol. 2014 Jun;133(3):575-83
pubmed: 24589413
Mol Biol Rep. 2014 Sep;41(9):6215-23
pubmed: 24985974
Cancer Lett. 2014 Dec 28;355(2):242-52
pubmed: 25218595
Mol Biol Int. 2014;2014:852748
pubmed: 25276427
Cancer Lett. 2016 Oct 1;380(2):568-76
pubmed: 26297987
J Biol Chem. 2016 Jan 15;291(3):1029-52
pubmed: 26534963
World J Surg Oncol. 2017 Mar 21;15(1):68
pubmed: 28327158
Am J Cancer Res. 2017 Feb 01;7(2):260-274
pubmed: 28337375
J Biol Chem. 2017 Aug 4;292(31):12772-12782
pubmed: 28615452
Sci Rep. 2018 Feb 21;8(1):3398
pubmed: 29467385

Auteurs

Xueyi Dong (X)

Department of Pathology, Tianjin Medical University, Tianjin 300070, P.R. China.
Department of Pathology, General Hospital of Tianjin Medical University, Tianjin 300052, P.R. China.

Yuheng Hong (Y)

School of Medical Imaging, Tianjin Medical University, Tianjin 300070, P.R. China.

Huizhi Sun (H)

Department of Pathology, Tianjin Medical University, Tianjin 300070, P.R. China.

Chen Chen (C)

Department of Pathology, Tianjin Medical University, Tianjin 300070, P.R. China.

Xiulan Zhao (X)

Department of Pathology, Tianjin Medical University, Tianjin 300070, P.R. China.
Department of Pathology, General Hospital of Tianjin Medical University, Tianjin 300052, P.R. China.

Baocun Sun (B)

Department of Pathology, Tianjin Medical University, Tianjin 300070, P.R. China.
Department of Pathology, General Hospital of Tianjin Medical University, Tianjin 300052, P.R. China.
Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China.

Classifications MeSH