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Placenta growth factor, PLGF, influences the motility of lung cancer cells, the role of Rho associated kinase, Rock1
Author(s) -
Chen Jinfeng,
Ye Lin,
Zhang Lijian,
Jiang Wen G.
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21831
Subject(s) - a549 cell , rock1 , placental growth factor , cancer research , angiogenesis , lung cancer , biology , microbiology and biotechnology , kinase , medicine , protein kinase a , vascular endothelial growth factor , vegf receptors
Placenta growth factor (PlGF) is a member of the VEGF family and has been implicated in the aggressive capacity of solid tumours, partly via its impact on angiogenesis. The present study determined the direct biological function of endogenous PlGF in lung cancer cells. From the human non‐small cell lung cancer cell line A549 which expressed good level of PlGF, we created sublines within which PlGF expression was knockdown by way of anti‐PlGF ribozyme transgenes. Remarkable reductions of both PlGF mRNA and protein by the ribozyme transgenes were revealed in A549 transfectants (A549 ΔPlGF ) using RT‐PCR and Western blotting respectively. A549 ΔPlGF cells exhibited significantly reduced migration and adhesion compared with the wild‐type (A549 WT ) and the empty plasmid control (A549 pEF/His ) cells. Immunocytochemistry and Western blotting further revealed that the expression of ROCK1, Rho associated kinase, was also reduced in A549 ΔPlGF cells, in comparison with wild‐type and control cells. In addition, A549 ΔPlGF cells lost its response to a ROCK inhibitor, which otherwise strongly inhibited the motility of A549 WT and A549 pEF/His cells. These data indicate that PlGF directly regulates the motility of human lung cancer cells and that this regulation critically dependent on ROCK‐1. The study further indicates that PlGF is a potential therapeutic target in lung cancer. J. Cell. Biochem. 105: 313–320, 2008. © 2008 Wiley‐Liss, Inc.