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

53 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).

UN SDGs

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

SDG 3 Good Health and Well-being

Keywords

Adhesion
Colon cancer cell
Integrin α2
Invasion
Migration
Syndecan-2

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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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doi = "10.1016/j.bbrc.2009.04.093",

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T1 - Syndecan-2 overexpression regulates adhesion and migration through cooperation with integrin α2

AU - Choi, Sojoong

AU - Kim, Yeonhee

AU - Park, Haein

AU - Han, Inn Oc

AU - Chung, Eunkyung

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).

PY - 2009/6/26

Y1 - 2009/6/26

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.

KW - Adhesion

KW - Colon cancer cell

KW - Integrin α2

KW - Invasion

KW - Migration

KW - Syndecan-2

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M3 - Article

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JF - Biochemical and Biophysical Research Communications

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ER -

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

Abstract

Bibliographical note

UN SDGs

Keywords

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