GPR56 promotes proliferation of colorectal cancer cells and enhances metastasis via epithelial‑mesenchymal transition through PI3K/AKT signaling activation

Ji,Bing; Feng,Yifei; Sun,Ye; Ji,Dongjian; Qian,Wenwei; Zhang,Zhiyuan; Wang,Qingyuan; Zhang,Yue; Zhang,Chuan; Sun,Yueming

doi:10.3892/or.2018.6582

GPR56 promotes proliferation of colorectal cancer cells and enhances metastasis via epithelial‑mesenchymal transition through PI3K/AKT signaling activation

Authors:
- Bing Ji
- Yifei Feng
- Ye Sun
- Dongjian Ji
- Wenwei Qian
- Zhiyuan Zhang
- Qingyuan Wang
- Yue Zhang
- Chuan Zhang
- Yueming Sun
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Affiliations: Department of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Department of Gastrointestinal Surgery, The First People's Hospital of Changzhou and The Third Affiliated Hospital of Suzhou University, Changzhou, Jiangsu 213003, P.R. China
Published online on: July 20, 2018 https://doi.org/10.3892/or.2018.6582
Pages: 1885-1896
Copyright: © Ji et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

G protein‑coupled receptor 56 (GPR56), a member of the orphan GPCR family, has been reported to be an oncogene in various malignancies. However, little is known regarding the detailed molecular mechanism of GPR56 in colorectal cancer (CRC). The present study aimed to detect the expression level and biological function of GPR56 in CRC. We examined the expression of GPR56 in CRC tissues and cell lines by quantitative real time (qRT)‑PCR, immunohistochemistry, and western blot analysis. The prognostic significance of GPR56 in CRC patients was evaluated by Kaplan‑Meier survival analysis. The influence of GPR56 on tumor cell proliferation (via Cell Counting Kit‑8, and a tumor formation assay in mice), apoptosis (flow cytometry), cell cycle distribution (flow cytometry) and migration (Transwell assay) was explored. We also investigated the underlying mechanism of GPR56 by western blot analysis. We found GPR56 expression was significantly upregulated in CRC tissues and cell lines compared to corresponding normal controls. Higher GPR56 expression in patients predicted poorer prognosis. Depletion of GPR56 markedly suppressed cell proliferation, migration, and invasion. GPR56 overexpression promoted CRC cell metastasis by expediting epithelial‑mesenchymal transition by activating PI3K/AKT signaling. In conclusion, GPR56 played an important role in CRC progression and may represent a new therapeutic target to reduce CRC metastasis.

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