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Dickkopf 2 promotes proliferation and invasion via Wnt signaling in prostate cancer
Wei Xu1, Kuan Pang1, Ze-Guang Zhou1
1Department of Urology, The First People's Hospital of Yulin, Yulin, Guangxi 537000, P.R. China.
Abstract:
Wnt/β-catenin signaling dysregulation is involved in tumorigenesis. Furthermore, epigenetic modification of the Dickkopf (DKK) family (DKK1‑4) has been shown to be important in the regulation of Wnt signaling. However, the functions and mechanism of DKK2 in the development and progression of prostate cancer remain unclear. Therefore, the present study investigated the role of DKK2 in prostate cancer. The mRNA and protein expression levels of DKK2 in prostate cancer tissues and cells were assessed by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The biological function of DKK2 in prostate cancer was investigated using 3‑(4,5‑dimethylthiazol‑2‑yl)-2,5‑diphenyltetrazolium bromide and transwell invasion assays. DKK2 was demonstrated to be upregulated in prostate cancer tissues and cells, and knockdown of DKK2 suppressed cell proliferation and invasion. Furthermore, small interfering RNA targeting DKK2 inhibited the expression of β‑catenin, cyclin D1 and c‑Myc in prostate cancer cells. The present report suggested that DKK2 downregulation suppressed the proliferation and invasion of prostate cancer cells by inhibiting the Wnt/β‑catenin signaling pathway.
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