Next Article in Journal
Evaluation and Management of Neurogenic Bladder: What Is New in China?
Next Article in Special Issue
Preliminary Evidence on the Diagnostic and Molecular Role of Circulating Soluble EGFR in Non-Small Cell Lung Cancer
Previous Article in Journal
SCM-198 Ameliorates Cognitive Deficits, Promotes Neuronal Survival and Enhances CREB/BDNF/TrkB Signaling without Affecting Aβ Burden in AβPP/PS1 Mice
Previous Article in Special Issue
Prognostic Value of Preoperative Serum Levels of Periostin (PN) in Early Breast Cancer (BCa)
Article Menu
Issue 8 (August) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2015, 16(8), 18564-18579; doi:10.3390/ijms160818564

Wnt3a Promotes the Vasculogenic Mimicry Formation of Colon Cancer via Wnt/β-Catenin Signaling

1,2,3,†
,
1,2,3,†
,
1,2,3
,
4
,
1,2,3,* and 1,2,3,4,*
1
Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China
2
The Key Laboratory of Tianjin Cancer Prevention and Treatment, Tianjin 300060, China
3
National Clinical Research Center for Cancer, Tianjin 300060, China
4
Department of Pathology, Tianjin Medical University, Tianjin 300070, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 12 July 2015 / Revised: 12 July 2015 / Accepted: 4 August 2015 / Published: 10 August 2015
(This article belongs to the Special Issue Molecular Classification of Human Cancer: Diagnosis and Treatment)
View Full-Text   |   Download PDF [1988 KB, uploaded 10 August 2015]   |  

Abstract

Our previous study provided evidence that non-canonical Wnt signaling is involved in regulating vasculogenic mimicry (VM) formation. However, the functions of canonical Wnt signaling in VM formation have not yet been explored. In this study, we found the presence of VM was related to colon cancer histological differentiation (p < 0.001), the clinical stage (p < 0.001), and presence of metastasis and recurrence (p < 0.001). VM-positive colon cancer samples showed increased Wnt3a expression (p < 0.001) and β-catenin nuclear expression (p < 0.001) compared with the VM-negative samples. In vitro, over-regulated Wnt3a expression in HT29 colon cancer cells promoted the capacity to form tube-like structures in the three-dimensional (3-D) culture together with increased expression of endothelial phenotype-associated proteins such as VEGFR2 and VE-cadherin. The mouse xenograft model showed that Wnt3a-overexpressing cells grew into larger tumor masses and formed more VM than the control cells. In addition, the Wnt/β-catenin signaling antagonist Dickkopf-1(Dkk1) can reverse the capacity to form tube-like structures and can decrease the expressions of VEGFR2 and VE-cadherin in Wnt3a-overexpressing cells. Taken together, our results suggest that Wnt/β-catenin signaling is involved in VM formation in colon cancer and might contribute to the development of more accurate treatment modalities aimed at VM. View Full-Text
Keywords: Wnt/β-catenin signaling; vasculogenic mimicry; Wnt3a; Dkk1; colon cancer Wnt/β-catenin signaling; vasculogenic mimicry; Wnt3a; Dkk1; colon cancer
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Qi, L.; Song, W.; Liu, Z.; Zhao, X.; Cao, W.; Sun, B. Wnt3a Promotes the Vasculogenic Mimicry Formation of Colon Cancer via Wnt/β-Catenin Signaling. Int. J. Mol. Sci. 2015, 16, 18564-18579.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top