FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients

Abstract Formyl peptide receptor 2 (FPR2), a classical chemoattractant receptor of G-protein-coupled receptors, is reported to be involved in invasion and metastasis of some cancers, but the role of FPR2 in gastric cancer (GC) has not yet been elucidated. In this study, we found that the levels of F...

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Autores principales:	Xi-Lu Hou, Cheng-Dong Ji, Jun Tang, Yan-Xia Wang, Dong-Fang Xiang, Hai-Qing Li, Wei-Wei Liu, Jiao-Xue Wang, He-Zhong Yan, Yan Wang, Peng Zhang, You-Hong Cui, Ji-Ming Wang, Xiu-Wu Bian, Wei Liu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5365e965aa6b40c58deb45b8004e9d84
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spelling	oai:doaj.org-article:5365e965aa6b40c58deb45b8004e9d842021-12-02T16:06:08ZFPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients10.1038/s41598-017-03368-72045-2322https://doaj.org/article/5365e965aa6b40c58deb45b8004e9d842017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03368-7https://doaj.org/toc/2045-2322Abstract Formyl peptide receptor 2 (FPR2), a classical chemoattractant receptor of G-protein-coupled receptors, is reported to be involved in invasion and metastasis of some cancers, but the role of FPR2 in gastric cancer (GC) has not yet been elucidated. In this study, we found that the levels of FPR2 expression in GC were positively correlated with invasion depth, lymph node metastasis and negatively correlated with the patients’ overall survival. Multivariate analysis indicated that FPR2 expression was an independent prognostic marker for GC patients. FPR2-knockdown significantly abrogated the migration and invasion stimulated by Hp(2–20) and Ac(2–26), two well-characterized ligands for FPR2 in GC cells. FPR2 deletion also reduced the tumorigenic and metastatic capabilities of GC cells in vivo. Mechanistically, stimulation with FPR2 ligands resulted in down-regulation of E-cadherin and up-regulation of vimentin, which were reversed by FPR2 knock-down, implying the involvement of epithelial–mesenchymal transition (EMT). Moreover, the activation of FPR2 was accompanied with ERK1/2 phosphorylation, which could be attenuated by FPR2 silencing or treatment with MEK inhibitor, PD98059. Altogether, our results demonstrate that FPR2 is functionally involved in invasion and metastasis, and potentially acts as a novel prognostic marker as well as a potential therapeutic target in human GC.Xi-Lu HouCheng-Dong JiJun TangYan-Xia WangDong-Fang XiangHai-Qing LiWei-Wei LiuJiao-Xue WangHe-Zhong YanYan WangPeng ZhangYou-Hong CuiJi-Ming WangXiu-Wu BianWei LiuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xi-Lu Hou Cheng-Dong Ji Jun Tang Yan-Xia Wang Dong-Fang Xiang Hai-Qing Li Wei-Wei Liu Jiao-Xue Wang He-Zhong Yan Yan Wang Peng Zhang You-Hong Cui Ji-Ming Wang Xiu-Wu Bian Wei Liu FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
description	Abstract Formyl peptide receptor 2 (FPR2), a classical chemoattractant receptor of G-protein-coupled receptors, is reported to be involved in invasion and metastasis of some cancers, but the role of FPR2 in gastric cancer (GC) has not yet been elucidated. In this study, we found that the levels of FPR2 expression in GC were positively correlated with invasion depth, lymph node metastasis and negatively correlated with the patients’ overall survival. Multivariate analysis indicated that FPR2 expression was an independent prognostic marker for GC patients. FPR2-knockdown significantly abrogated the migration and invasion stimulated by Hp(2–20) and Ac(2–26), two well-characterized ligands for FPR2 in GC cells. FPR2 deletion also reduced the tumorigenic and metastatic capabilities of GC cells in vivo. Mechanistically, stimulation with FPR2 ligands resulted in down-regulation of E-cadherin and up-regulation of vimentin, which were reversed by FPR2 knock-down, implying the involvement of epithelial–mesenchymal transition (EMT). Moreover, the activation of FPR2 was accompanied with ERK1/2 phosphorylation, which could be attenuated by FPR2 silencing or treatment with MEK inhibitor, PD98059. Altogether, our results demonstrate that FPR2 is functionally involved in invasion and metastasis, and potentially acts as a novel prognostic marker as well as a potential therapeutic target in human GC.
format	article
author	Xi-Lu Hou Cheng-Dong Ji Jun Tang Yan-Xia Wang Dong-Fang Xiang Hai-Qing Li Wei-Wei Liu Jiao-Xue Wang He-Zhong Yan Yan Wang Peng Zhang You-Hong Cui Ji-Ming Wang Xiu-Wu Bian Wei Liu
author_facet	Xi-Lu Hou Cheng-Dong Ji Jun Tang Yan-Xia Wang Dong-Fang Xiang Hai-Qing Li Wei-Wei Liu Jiao-Xue Wang He-Zhong Yan Yan Wang Peng Zhang You-Hong Cui Ji-Ming Wang Xiu-Wu Bian Wei Liu
author_sort	Xi-Lu Hou
title	FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
title_short	FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
title_full	FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
title_fullStr	FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
title_full_unstemmed	FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
title_sort	fpr2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/5365e965aa6b40c58deb45b8004e9d84
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FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients

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