Kisspeptin-10, a KISS1-derived decapeptide, inhibits tumor angiogenesis by suppressing Sp1-mediated VEGF expression and FAK/Rho GTPase activation.

In the chicken chorioallantoic membrane assay, kisspeptin‑10 inhibited angiogenesis.

In plain wordsIn chicken embryo membrane tests, kisspeptin‑10 reduced new blood-vessel growth.

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In the VEGF-induced mouse corneal micropocket assay, kisspeptin‑10 inhibited angiogenesis.

In plain wordsIn mice, kisspeptin‑10 reduced new blood-vessel growth in the cornea.

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In SCID mice xenografted with human prostate cancer cells (PC-3), kisspeptin‑10 inhibited tumor growth.

In plain wordsIn mice with human prostate tumor grafts, kisspeptin‑10 slowed tumor growth.

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In SCID mice xenografted with PC-3 cells, kisspeptin‑10 inhibited tumor angiogenesis, which the abstract links to its inhibition of tumor growth.

In plain wordsIn mice with human prostate tumor grafts, kisspeptin‑10 reduced tumor blood-vessel growth.

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In human umbilical vein endothelial cells, kisspeptin‑10 significantly inhibited migration.

In plain wordsIn cells, kisspeptin‑10 reduced the movement of human blood-vessel lining cells.

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In human umbilical vein endothelial cells, kisspeptin‑10 significantly inhibited invasion.

In plain wordsIn cells, kisspeptin‑10 reduced the invasion of human blood-vessel lining cells.

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In human umbilical vein endothelial cells, kisspeptin‑10 significantly inhibited tube formation.

In plain wordsIn cells, kisspeptin‑10 reduced tube formation by human blood-vessel lining cells.

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In human umbilical vein endothelial cells, kisspeptin‑10 had little effect on proliferation.

In plain wordsIn cells, kisspeptin‑10 had little effect on the growth of human blood-vessel lining cells.

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In human prostate cancer cells, kisspeptin‑10 had little effect on proliferation.

In plain wordsIn cells, kisspeptin‑10 had little effect on the growth of human prostate cancer cells.

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In human umbilical vein endothelial cells, kisspeptin‑10 suppressed VEGF expression.

In plain wordsIn cells, kisspeptin‑10 reduced the level of VEGF, a blood-vessel growth signal.

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In human umbilical vein endothelial cells, kisspeptin‑10 inhibited the binding of specificity protein 1 to the VEGF promoter.

In plain wordsIn cells, kisspeptin‑10 reduced binding of a gene-control protein to the VEGF gene switch.

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In human umbilical vein endothelial cells, kisspeptin‑10 blocked activation of the c-Src/focal adhesion kinase signaling pathway.

In plain wordsIn cells, kisspeptin‑10 blocked a signaling pathway, c-Src/focal adhesion kinase, in blood-vessel lining cells.

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In human umbilical vein endothelial cells, kisspeptin‑10 blocked activation of Rac/Cdc42 signaling.

In plain wordsIn cells, kisspeptin‑10 blocked Rac/Cdc42 signaling in blood-vessel lining cells.

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