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Here, we showed that in ovarian cancer CXCL12 induced EMT phenotypes including the spindle\u2010like cell morphology, podia and stress fiber formation, a decrease in E\u2010cadherin expression, and increases in mesenchymal N\u2010cadherin and vimentin expressions. These effects of CXCL12 could be antagonized by the CXCR4 antagonist AMD3100, but not by the anti\u2010CXCR7 antibody. The expressions of the EMT markers were significantly down\u2010regulated by the CXCR4 siRNA, and up\u2010regulated by the pcDNA3.1\/CXCR4 plasmid, whereas not affected by the CXCR7 siRNA. Furthermore, intraperitoneal administration of AMD3100 inhibited tumor dissemination and growth in the nude mice inoculated with ovarian IGROV\u20101 cells with a concomitant reduction in EMT marker expressions. Collectively, these data suggest that CXCR4, rather than CXCR7, plays a key role in CXCL12\u2010activated EMT phenotypes, and targeting the CXCL12\u2010CXCR4 chemokine axis represents a potential therapeutic strategy to prevent ovarian cancer progression.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mc.22916","type":"journal-article","created":{"date-parts":[[2018,9,27]],"date-time":"2018-09-27T06:58:51Z","timestamp":1538031531000},"page":"144-155","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["CXCR7 is not obligatory for CXCL12\u2010CXCR4\u2010induced epithelial\u2010mesenchymal transition in human ovarian cancer"],"prefix":"10.1002","volume":"58","author":[{"given":"Ning","family":"Zheng","sequence":"first","affiliation":[{"name":"Cancer Metastasis Alert and Prevention Center, and Biopharmaceutical Photocatalysis State Key Laboratory of Photocatalysis on Energy and Environment College of Chemistry, Fuzhou University 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