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HOXD3-overexpression increases integrin alphavbeta3 expression and deprives E-cadherin while it enhances cell motility in A549 cells.

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Title: HOXD3-overexpression increases integrin alphavbeta3 expression and deprives E-cadherin while it enhances cell motility in A549 cells.
Authors: Ohta, Hironori Browse this author
Hamada, Jun-ichi Browse this author
Tada, Mitsuhiro Browse this author
Aoyama, Tetsuya Browse this author
Furuuchi, Keiji Browse this author
Takahashi, Yoko Browse this author
Totsuka, Yasunori Browse this author
Moriuchi, Tetsuya Browse this author
Keywords: Haptotaxis
E-cadherin
HOXD3
Integrin αvβ3
Migration
Phagokinesis
Wound-healing assay
Issue Date: Dec-2006
Publisher: Springer
Journal Title: Clinical & Experimental Metastasis
Volume: 23
Issue: 7-8
Start Page: 381
End Page: 390
Publisher DOI: 10.1007/s10585-006-9047-5
PMID: 17187229
Abstract: We have previously shown that transduction of HOXD3, one of homeobox genes, into human lung cancer A549 cells enhances cell motility, invasion and metastasis. In the present study, we examined the roles of integrin β3 which was up-regulated by HOXD3-overexpression in the HOXD3-induced motility of A549 cells. We first established integrin β3-transfectants and compared their motile activity to those of the HOXD3-transfected, control-transfected and parental cells by three different assays. The integrin β3-transfectants as well as the HOXD3-transfectants formed heterodimer with integrin αv subunit, and showed highly motile activities assessed by haptotaxis or phagokinetic track assay compared to the control transfectants or parental cells. In vitro wound-healing assay revealed that migratory activities were graded as the HOXD3-transfectants > the integrin β3-transfectants > the control transfectants or parental cells. E-cadherin was expressed in the integrin β3-transfectants but not expressed in the HOXD3-transfectants. An addition of function-blocking antibody to E-cadherin into the wound-healing assay promoted the migratory activity of the integrin β3-transfectants, suggesting that E-cadherin prevented the cells from dissociating from the wound edges. These results indicate that increased expression of integrin αv β3 and loss of E-cadherin by HOXD3-overexpression are responsible for the enhanced motility and dissociation.
Rights: The original publication is available at www.springerlink.com
Type: article (author version)
URI: http://hdl.handle.net/2115/18952
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 浜田 淳一

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