| Literature DB >> 26166822 |
Ting Wang1, Shuai Han1, Zhipeng Wu1, Zhitao Han1, Wangjun Yan1, Tielong Liu1, Haifeng Wei1, Dianwen Song1, Wang Zhou2, Xinghai Yang3, Jianru Xiao4.
Abstract
Bone metastasis occurs in approximately 30-40% patients with advanced non-small cell lung cancer (NSCLC), but the mechanism underlying this bone metastasis remains poorly understood. The chemokine super family is believed to play an important role in tumor metastasis in lung cancer. The chemokine receptor XCR1 has been identified to promote cell proliferation and migration in oral cancer and ovarian carcinoma, but the role of XCR1 in lung cancer has not been reported. In this study, we demonstrated for the first time that XCR1 was overexpressed in lung cancer bone metastasis as compared with that in patients with primary lung cancer. In addition, the XCR1 ligand XCL1 promoted the proliferation and migration of lung cancer cells markedly, and knockdown of XCR1 by siRNA abolished the effect of XCL1 in cell proliferation and migration. Furthermore, we identified JAK2/STAT3 as a novel downstream pathway of XCR1, while XCL1/XCR1 increased the mRNA level of the downstream of JAK2/STAT3 including PIM1, JunB, TTP, MMP2 and MMP9. These results indicate that XCR1 is a new potential therapeutic target for the treatment of lung cancer bone metastasis.Entities:
Keywords: Bone metastasis; Cell migration; Cell proliferation; JAK2/STAT3 pathway; Non-small cell lung cancer (NSCLC); XCR1
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Year: 2015 PMID: 26166822 DOI: 10.1016/j.bbrc.2015.06.175
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575