Abstract
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.
Highlights
61,560 Americans are expected to be diagnosed with cancer of the kidney and renal pelvis in 2015, and 14,080 deaths are predicted to be related to this disease [1]
Since TIKI2 was upregulated in renal cell carcinoma (RCC) specimens and cell lines, we investigated the role of TIKI2 on RCC cell behaviors
Here www.impactjournals.com/oncotarget we investigated the role of TIKI2 in RCC and discovered for the first time that TIKI2 is highly expressed in human RCC specimens and could promote RCC growth
Summary
61,560 Americans are expected to be diagnosed with cancer of the kidney and renal pelvis in 2015, and 14,080 deaths are predicted to be related to this disease [1]. Targeted therapies such as vascular endothelial growth factor and mammalian target of rapamycin inhibitors have transformed the management of metastatic renal cell carcinoma (RCC), these drugs have shown limited efficacy and metastatic RCC remains incurable [2]. There has been much interest in investigating the other important signaling pathways involved in the pathogenesis of RCC. Wnt signaling regulates some other pathways that have not yet been extensively elucidated
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