Syndecan-2 overexpression regulates adhesion and migration through cooperation with integrin α2

Sojoong Choi; Yeonhee Kim; Haein Park; Inn Oc Han; Eunkyung Chung; Sung Yul Lee; Yong Bae Kim; Jung Weon Lee; Eok Soo Oh; Jae Youn Yi

doi:10.1016/j.bbrc.2009.04.093

Syndecan-2 overexpression regulates adhesion and migration through cooperation with integrin α2

Sojoong Choi, Yeonhee Kim, Haein Park, Inn Oc Han, Eunkyung Chung, Sung Yul Lee, Yong Bae Kim, Jung Weon Lee, Eok Soo Oh, Jae Youn Yi

Department of Life Science

Research output: Contribution to journal › Article › peer-review

51 Scopus citations

Abstract

Syndecan-2, a transmembrane heparan sulfate proteoglycan, is known to serve as an adhesion receptor, but details of the regulatory mechanism governing syndecan-2 cell adhesion and migration remain unclear. Here, we examined this regulatory mechanism, showing that overexpression of syndecan-2 enhanced collagen adhesion, cell migration and invasion of normal rat intestinal epithelial cells (RIE1), and increased integrin α2 expression levels. Interestingly, RIE1 cells transfected with either syndecan-2 or integrin α2 showed similar adhesion and migration patterns, and a function-blocking anti-integrin α2 antibody abolished syndecan-2-mediated adhesion and migration. Consistent with these findings, transfection of integrin α2 siRNA diminished syndecan-2-induced cell migration in HCT116 human colon cancer cells. Taken together, these results demonstrate a novel cooperation between syndecan-2 and integrin α2β1 in adhesion-mediated cell migration and invasion. This interactive dynamic might be a possible mechanism underlying the tumorigenic activities of colon cancer cells.

Original language	English
Pages (from-to)	231-235
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	384
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2009.04.093
State	Published - 26 Jun 2009

Bibliographical note

Funding Information:
This study was supported by the National R&D Program for Cancer Control of the Korean Ministry of Health & Welfare (0420070-1 to E.S.O.), a Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund, KRF-2006-003-C00220), and the National Nuclear Research & Development Program of the Korean Ministry of Science and Technology (2007-00324).

Keywords

Adhesion
Colon cancer cell
Integrin α2
Invasion
Migration
Syndecan-2

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2009.04.093

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title = "Syndecan-2 overexpression regulates adhesion and migration through cooperation with integrin α2",

abstract = "Syndecan-2, a transmembrane heparan sulfate proteoglycan, is known to serve as an adhesion receptor, but details of the regulatory mechanism governing syndecan-2 cell adhesion and migration remain unclear. Here, we examined this regulatory mechanism, showing that overexpression of syndecan-2 enhanced collagen adhesion, cell migration and invasion of normal rat intestinal epithelial cells (RIE1), and increased integrin α2 expression levels. Interestingly, RIE1 cells transfected with either syndecan-2 or integrin α2 showed similar adhesion and migration patterns, and a function-blocking anti-integrin α2 antibody abolished syndecan-2-mediated adhesion and migration. Consistent with these findings, transfection of integrin α2 siRNA diminished syndecan-2-induced cell migration in HCT116 human colon cancer cells. Taken together, these results demonstrate a novel cooperation between syndecan-2 and integrin α2β1 in adhesion-mediated cell migration and invasion. This interactive dynamic might be a possible mechanism underlying the tumorigenic activities of colon cancer cells.",

keywords = "Adhesion, Colon cancer cell, Integrin α2, Invasion, Migration, Syndecan-2",

author = "Sojoong Choi and Yeonhee Kim and Haein Park and Han, {Inn Oc} and Eunkyung Chung and Lee, {Sung Yul} and Kim, {Yong Bae} and Lee, {Jung Weon} and Oh, {Eok Soo} and Yi, {Jae Youn}",

note = "Funding Information: This study was supported by the National R&D Program for Cancer Control of the Korean Ministry of Health & Welfare (0420070-1 to E.S.O.), a Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund, KRF-2006-003-C00220), and the National Nuclear Research & Development Program of the Korean Ministry of Science and Technology (2007-00324). ",

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AU - Kim, Yeonhee

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AU - Lee, Sung Yul

AU - Kim, Yong Bae

AU - Lee, Jung Weon

AU - Oh, Eok Soo

AU - Yi, Jae Youn

N1 - Funding Information: This study was supported by the National R&D Program for Cancer Control of the Korean Ministry of Health & Welfare (0420070-1 to E.S.O.), a Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund, KRF-2006-003-C00220), and the National Nuclear Research & Development Program of the Korean Ministry of Science and Technology (2007-00324).

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N2 - Syndecan-2, a transmembrane heparan sulfate proteoglycan, is known to serve as an adhesion receptor, but details of the regulatory mechanism governing syndecan-2 cell adhesion and migration remain unclear. Here, we examined this regulatory mechanism, showing that overexpression of syndecan-2 enhanced collagen adhesion, cell migration and invasion of normal rat intestinal epithelial cells (RIE1), and increased integrin α2 expression levels. Interestingly, RIE1 cells transfected with either syndecan-2 or integrin α2 showed similar adhesion and migration patterns, and a function-blocking anti-integrin α2 antibody abolished syndecan-2-mediated adhesion and migration. Consistent with these findings, transfection of integrin α2 siRNA diminished syndecan-2-induced cell migration in HCT116 human colon cancer cells. Taken together, these results demonstrate a novel cooperation between syndecan-2 and integrin α2β1 in adhesion-mediated cell migration and invasion. This interactive dynamic might be a possible mechanism underlying the tumorigenic activities of colon cancer cells.

AB - Syndecan-2, a transmembrane heparan sulfate proteoglycan, is known to serve as an adhesion receptor, but details of the regulatory mechanism governing syndecan-2 cell adhesion and migration remain unclear. Here, we examined this regulatory mechanism, showing that overexpression of syndecan-2 enhanced collagen adhesion, cell migration and invasion of normal rat intestinal epithelial cells (RIE1), and increased integrin α2 expression levels. Interestingly, RIE1 cells transfected with either syndecan-2 or integrin α2 showed similar adhesion and migration patterns, and a function-blocking anti-integrin α2 antibody abolished syndecan-2-mediated adhesion and migration. Consistent with these findings, transfection of integrin α2 siRNA diminished syndecan-2-induced cell migration in HCT116 human colon cancer cells. Taken together, these results demonstrate a novel cooperation between syndecan-2 and integrin α2β1 in adhesion-mediated cell migration and invasion. This interactive dynamic might be a possible mechanism underlying the tumorigenic activities of colon cancer cells.

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Syndecan-2 overexpression regulates adhesion and migration through cooperation with integrin α2

Abstract

Bibliographical note

Keywords

UN SDGs

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