Downregulation of Wnt3 Suppresses Colorectal Cancer Development Through Inhibiting Cell Proliferation and Migration

Xiaobo Nie; Fulin Xia; Ying Liu; Yun Zhou; Wenling Ye; Panha Hean; Jiming Meng; Huiyang Liu; Lei Liu; Jianxun Wen; Xuequn Ren; Wei-Dong Chen; Yan-Dong Wang

doi:10.3389/fphar.2019.01110

Downregulation of Wnt3 Suppresses Colorectal Cancer Development Through Inhibiting Cell Proliferation and Migration

Front Pharmacol. 2019 Oct 1:10:1110. doi: 10.3389/fphar.2019.01110. eCollection 2019.

Authors

Xiaobo Nie¹, Fulin Xia¹, Ying Liu¹, Yun Zhou¹, Wenling Ye¹, Panha Hean², Jiming Meng², Huiyang Liu¹, Lei Liu¹, Jianxun Wen³, Xuequn Ren², Wei-Dong Chen^{1

3}, Yan-Dong Wang⁴

Affiliations

¹ Key Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University, Kaifeng, China.
² Department of General Surgery, Affiliated Huaihe Hospital of Henan University, Kaifeng, China.
³ Key Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot, China.
⁴ State Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, China.

Abstract

The aberrant expression of Wnt3 has linked to several types of human malignancies. However, it is not known for its role in tumorigenesis of colorectal cancer (CRC). Herein, we show that Wnt3 is upregulated in human CRC tissues and is essential for the CRC progression. Knockdown of Wnt3 in human CRC cells delayed tumor formation in nude mouse xenografts through silencing of canonical Wnt pathway and glycolysis. We further found that silencing of Wnt3 enhanced the sensitivity of CRC cells to cisplatin through inducing apoptotic cell death. Taken together, it demonstrates that Wnt3 is a novel clinical biomarker for the detection of CRC and plays an important role in colorectal tumorigenesis. Therefore, downregulation of Wnt3 will be a valuable strategy in CRC treatment.

Keywords: HCT-116; Wnt3; apoptosis; colorectal cancer; glycolysis; proliferation.