Open Access

ARTICLE

Silencing of Armadillo Repeat-Containing Protein 8 (ARMc8) Inhibits TGF-β-Induced EMT in Bladder Carcinoma UMUC3 Cells

Xuan Liang^*, Qun-Li Men^†, Yong-wei Li^‡, He-Cheng Li^§, Tie Chong^§, Zhao-lun Li^§

* Department of Oncology, The First Affiliated Hospital, Xi’an Jiaotong University Medical College, Xi’an, Shaanxi, P.R. China
† Department of Urology, The Central Hospital of Baoji, Baoji, Shaanxi, P.R. China
‡ Department of Urology, The Central Hospital of Weinan, Weinan, Shaanxi, P.R. China
§ Department of Urology, The Second Affiliated Hospital, Xi’an Jiaotong University Medical College, Xi’an, Shaanxi, P.R. China

Oncology Research 2017, 25(1), 99-105. https://doi.org/10.3727/096504016X14719078133609

Abstract

Armadillo repeat-containing protein 8 (ARMc8) is a key factor in regulating cell migration, proliferation, tissue maintenance, and tumorigenesis. However, its role in bladder cancer remains unknown. Thus, in this study we sought to investigate the effect of ARMc8 on the epithelial-to-mesenchymal transition (EMT) progress in bladder cancer cells induced by transforming growth factor-b1 (TGF-β1). Our results found that ARMc8 was highly expressed in bladder cancer cell lines. ARMc8 silencing inhibited the TGF-β1-induced migration and invasion and suppressed the EMT progress in bladder cancer cells. Furthermore, ARMc8 silencing inhibited the TGF-β1-induced expression of β-catenin, cyclin D1, and c-myc in bladder cancer cells. In conclusion, the present study demonstrates a novel function for ARMc8, which acts as a mediator for TGF-β1-induced cell migration/invasion through modulation of the Wnt/β-catenin signaling pathway in bladder cancer cells. This study suggests that ARMc8 may be a potential therapeutic target for the development of therapies for bladder cancer.

---

Keywords

---