GPR171 expression enhances proliferation and metastasis of lung cancer cells
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So Hee Dho1,2, Kwang-Pyo Lee1, Dongjun Jeong3, Chang-Jin Kim3, Kyung-Sook Chung4, Ji Young Kim1, Bum-Chan Park1, Sung Sup Park1, Seon-Young Kim4,5, Ki-Sun Kwon1,5
1Aging Research Institute, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea
2Radioisotope Research Division, Department of Research Reactor Utilization, Korea Atomic Energy Research Institute, Daejeon 305-353, Republic of Korea
3Department of Pathology, College of Medicine Soonchunhyang University, Chonan 330-090, Republic of Korea
4Genome Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea
5Department of Functional Genomics, Korea University of Science and Technology (UST), Daejeon 305-333, Republic of Korea
Ki-Sun Kwon, e-mail: email@example.com
Keywords: GPCR, GPR171, EGFR, lung cancer
Received: August 03, 2015 Accepted: January 02, 2016 Published: January 09, 2016
G protein-coupled receptors (GPCRs) are among the most significant therapeutic targets and some of them promote the growth and metastasis of cancer. Here, we show that an increase in the levels of GPR171 is crucial for lung cancer tumor progression in vitro and in vivo. Immunostaining of clinical samples indicated that GPR171 was overexpressed in 46.8% of lung carcinoma tissues. Depletion of GPR171 with an anti-GPR171 antibody decreased proliferation of lung carcinoma cells and attenuated tumor progression in a mouse xenograft model. Knockdown of GPR171 also inhibited migration and invasion of the lung cancer cell lines. Notably, inhibition of GPR171 synergistically enhanced the tumoricidal activity of an epidermal growth factor receptor (EGFR) inhibitor in lung cancer cells. These results indicate that GPR171 blockade is a promising antineoplastic strategy and provide a preclinical rationale for combined inhibition of GPR171 and EGFR.
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