title: Endocrine gland-derived vascular endothelial growth factor strengthens             cell invasion ability via prokineticin receptor 2 in colon cancer cell lines.
abstract: Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) has             recently been identified as one of the vascular endothelial growth factors, and             it is considered that the overexpression of EG-VEGF in colon cancer is related             to hepatic metastasis. In this study, we report our recent novel findings of the             involvement of EG-VEGF in cell invasion of colon cancer cells. Colon cancer cell             lines (DLD-1 and HCT116) with high expression of prokineticin receptor (PK-R)             1 and 2 were stimulated with the EG-VEGF protein. Furthermore, Matrigel cell invasion             assay was performed to examine the changes in cancer cell invasion. In addition,             we investigated the mRNA expression of matrix metalloproteinase (MMP)-2, -7 and             -9 in cancer cells. Finally, the EG-VEGF receptor on the colon cancer cell membrane             was blocked by anti-PK-R1 and -PK-R2 antibodies to study whether cell invasion             ability would be altered. In colon cancer cell lines where the expression of PK-R1             and 2 was confirmed, stimulation with EG-VEGF increased cell invasion a maximum             of ~3-5 times. Furthermore, an increase in the mRNA and protein expression of             MMP-2, -7 and -9 was observed. We also observed that the cell invasion rate decreased             only after exposure to the anti-PK-R2 antibody. The study showed that the EG-VEGF             protein may act on MMP-2, -7 and -9 via PK-R2 to strengthen cell invasion ability             in colon cancer cell lines.
authors.affiliation: First Department of Surgery, University of Fukui, Yoshida-gun,                     Fukui, Japan.
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Tabata
authors.forename: Takanori
authors.initials: T
authors.lastname: Goi
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Nakazawa
authors.forename: Youhei
authors.initials: Y
authors.lastname: Kimura
authors.forename: Kanji
authors.initials: K
authors.lastname: Katayama
authors.forename: Akio
authors.initials: A
authors.lastname: Yamaguchi
mesh_terms: D000906:Antibodies / Q000494:pharmacology; D002465:Cell Movement / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D005768:Gastrointestinal Hormones / Q000276:immunology / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects; D045325:HCT116 Cells; D006801:Humans; D020778:Matrix Metalloproteinase 2 / Q000235:genetics; D020783:Matrix Metalloproteinase 7 / Q000235:genetics; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D009361:Neoplasm Invasiveness; D012333:RNA, Messenger / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000276:immunology / Q000378:metabolism*; D018000:Receptors, Peptide / Q000276:immunology / Q000378:metabolism*; D042662:Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D000906:Antibodies; D005768:Gastrointestinal Hormones; C467610:PROK1 protein, human; C470838:PROKR2 protein, human; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; D018000:Receptors, Peptide; D042662:Vascular Endothelial Growth Factor, Endocrine-Gland-Derived; D020783:Matrix Metalloproteinase 7; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9