TIKI2 is upregulated and plays an oncogenic role in renal cell carcinoma
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Xiaodong Yuan1,*, Baijun Dong1,*, Yunze Xu1, Liang Dong1, Jiwei Huang1, Jin Zhang1, Yonghui Chen1, Wei Xue1, Yiran Huang1
1Department of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China
*These authors have contributed equally to this work
Yiran Huang, e-mail: email@example.com
Keywords: TIKI2, renal cell carcinoma, Wnt antagonist, β-catenin, Wnt
Received: November 17, 2015 Accepted: February 11, 2016 Published: March 03, 2016
TIKI2 is a negative regulator of the Wnt family. Although many Wnt antagonists play important roles in renal cell carcinoma (RCC), the molecular function of TIKI2 in human RCC has not been fully elucidated. Here, we analyzed TIKI2 mRNA level in RCC specimens, the corresponding non-tumor tissues, RCC cell lines, and human proximal tubule epithelial cell line HK-2 using qPCR. We demonstrated that TIKI2 was highly expressed in RCC tissue (P < 0.05) and most RCC cell lines. In vitro, TIKI2 knockdown significantly inhibited proliferation, invasion, and clone formation ability of 769-P cells compared with controls, while ectopic TIKI2 expression enhanced A498 cell proliferation, invasion, and clone formation ability. In vivo, the average tumor volume was significantly increased in mice injected with A498-Tiki2 cells (P < 0.05). In the 769-P cell TIKI2 knockdown group, the average tumor volume was not significantly different compared to that of the control group (P = 0.08). Moreover, Wnt/β-catenin signaling was not affected by TIKI2 knockdown or overexpression. Results of the present study indicate that TIKI2 is upregulated in RCC tissues and plays an oncogenic role in RCC.
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