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• W2894176893 abstract "Although the CXCL12‐CXCR4/CXCR7 chemokine axis is demonstrated to play an integral role in tumor progression, the controversy exists and the role of CXCL12‐CXCR4/CXCR7 signaling axis in epithelial‐mesenchymal transition (EMT) of human ovarian cancer has not been explored. Here, we showed that in ovarian cancer CXCL12 induced EMT phenotypes including the spindle‐like cell morphology, podia and stress fiber formation, a decrease in E‐cadherin expression, and increases in mesenchymal N‐cadherin and vimentin expressions. These effects of CXCL12 could be antagonized by the CXCR4 antagonist AMD3100, but not by the anti‐CXCR7 antibody. The expressions of the EMT markers were significantly down‐regulated by the CXCR4 siRNA, and up‐regulated 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‐1 cells with a concomitant reduction in EMT marker expressions. Collectively, these data suggest that CXCR4, rather than CXCR7, plays a key role in CXCL12‐activated EMT phenotypes, and targeting the CXCL12‐CXCR4 chemokine axis represents a potential therapeutic strategy to prevent ovarian cancer progression." @default.
• W2894176893 created "2018-10-05" @default.
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• W2894176893 date "2018-10-16" @default.
• W2894176893 modified "2023-10-15" @default.
• W2894176893 title "CXCR7 is not obligatory for CXCL12‐CXCR4‐induced epithelial‐mesenchymal transition in human ovarian cancer" @default.
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• W2894176893 doi "https://doi.org/10.1002/mc.22916" @default.
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• W2894176893 hasPublicationYear "2018" @default.
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