NDLI: Opposite roles of LPA1 and LPA3 on cell motile and invasive activities of pancreatic cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kato, Kohei Yoshikawa, Kyohei Tanabe, Eriko Kitayoshi, Misaho Fukui, Rie Fukushima, Nobuyuki Tsujiuchi, Toshifumi
Description	Country affiliation: Japan Author Affiliation: Kato K ( Division of Cancer Biology and Bioinformatics, Department of Life Science, Faculty of Science and Engineering, Kinki University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.)
Abstract	Lysophosphatidic acid (LPA) interacts with at least six G protein-coupled transmembrane LPA receptors. Recently, it has been demonstrated that each LPA receptor acts as a positive or negative regulator of cellular function. In the present study, to assess a biological role of LPA receptors on cell migration of pancreatic cancer cells, we generated LPA receptor-1 (LPA(1)) and LPA(3) knockdown cells from hamster pancreatic cancer cells by transfection with short hairpin RNA plasmids and measured their cell motile and invasive abilities. In cell motility and invasion assay, a Cell Culture Insert, coated with or without a Matrigel, was used. While the cell motility and invasion of Lpar1 knockdown cells were markedly enhanced than those of control cells, Lpar3 knockdown cells showed significantly lower cell motility and invasion. Moreover, to investigate an involvement of LPA(1) and LPA(3) in the development of pancreatic cancers, we also measured the expression levels of Lpar1 and Lpar3 genes in hamster pancreatic duct adenocarcinomas (PDAs) induced by a nitroso compound. The expressions of Lpar1 gene in PDAs were significantly lower than those in normal pancreatic tissues. By contrast, the elevated expressions of Lpar3 gene were detected in PDAs. We thus demonstrate that LPA(1) and LPA(3) play the different roles on cell migration ability of pancreatic cancer cells, suggesting the opposite effects via LPA(1) and LPA(3) may contribute to the pathogenesis of pancreatic cancers in hamsters.
File Format	HTM / HTML
ISSN	10104283
Issue Number	5
Volume Number	33
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2012-10-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Cell Movement Pancreatic Neoplasms Pathology Receptors, Lysophosphatidic Acid Physiology Animals Cell Line, Tumor Drug Effects Cricetinae Gene Knockdown Techniques Lysophospholipids Pharmacology Neoplasm Invasiveness Genetics Metabolism Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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