Invadopodia formation in oral squamous cell carcinoma

The role of epidermal growth factor receptor signalling

Young Sun Hwang, Kwang Kyun Park, WonYoon Chung

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Objective: Invadopodia are actin-rich structures that are formed on the ventral membrane of the cell and degrade extracellular matrix (ECM) by accumulation of matrix metalloproteinase (MMP). Consequently, understanding how invadopodia form and function should facilitate the identification of new therapeutic target for anti-invadopodia therapy. The present study was designed to investigate invadopodia formation associated with oral squamous cell carcinoma (OSCC) and the effect of epidermal growth factor receptor (EGFR) signalling on invadopodia formation and ECM degradation activity. Design: Immunofluorescence analysis of invadopodia formation and ECM degradation was performed using confocal microscope. To understand the role of EGFR signalling, cells were treated with AG1478 or PD153035 (EGF receptor tyrosine kinase inhibitors) and assessed using zymography and an ECM degradation assay. Results: Invadopodia containing dot-shaped F-actin were observed in stress fibres of HSC-3 OSCC along with evidence of ECM degradation activity. GM6001, a broad range of MMP inhibitor impaired matrix degradation and gelatinolytic activity of active MMP-2. AG1478 and PD153035 inhibited invadopodia formation and ECM degradation activity, as well as gelatinolytic activity of proMMP-9 and proMMP-2. Conclusions: We provide evidence that HSC-3 OSCC has a tendency to adopt invadopodia for invasion and accompanying MMP-dependent proteolytic ECM degradation and EGFR signalling is necessary for invadopodia formation and associated ECM degradation activity.

Original languageEnglish
Pages (from-to)335-343
Number of pages9
JournalArchives of Oral Biology
Volume57
Issue number4
DOIs
Publication statusPublished - 2012 Apr 1

Fingerprint

Epidermal Growth Factor Receptor
Squamous Cell Carcinoma
Extracellular Matrix
Matrix Metalloproteinases
Actins
Podosomes
Stress Fibers
Matrix Metalloproteinase Inhibitors
Matrix Metalloproteinase 2
Protein-Tyrosine Kinases
Fluorescent Antibody Technique
Cell Membrane
Therapeutics

All Science Journal Classification (ASJC) codes

  • Otorhinolaryngology
  • Cell Biology
  • Dentistry(all)

Cite this

@article{e4b85041b0ec46f0813d004affd04cb5,
title = "Invadopodia formation in oral squamous cell carcinoma: The role of epidermal growth factor receptor signalling",
abstract = "Objective: Invadopodia are actin-rich structures that are formed on the ventral membrane of the cell and degrade extracellular matrix (ECM) by accumulation of matrix metalloproteinase (MMP). Consequently, understanding how invadopodia form and function should facilitate the identification of new therapeutic target for anti-invadopodia therapy. The present study was designed to investigate invadopodia formation associated with oral squamous cell carcinoma (OSCC) and the effect of epidermal growth factor receptor (EGFR) signalling on invadopodia formation and ECM degradation activity. Design: Immunofluorescence analysis of invadopodia formation and ECM degradation was performed using confocal microscope. To understand the role of EGFR signalling, cells were treated with AG1478 or PD153035 (EGF receptor tyrosine kinase inhibitors) and assessed using zymography and an ECM degradation assay. Results: Invadopodia containing dot-shaped F-actin were observed in stress fibres of HSC-3 OSCC along with evidence of ECM degradation activity. GM6001, a broad range of MMP inhibitor impaired matrix degradation and gelatinolytic activity of active MMP-2. AG1478 and PD153035 inhibited invadopodia formation and ECM degradation activity, as well as gelatinolytic activity of proMMP-9 and proMMP-2. Conclusions: We provide evidence that HSC-3 OSCC has a tendency to adopt invadopodia for invasion and accompanying MMP-dependent proteolytic ECM degradation and EGFR signalling is necessary for invadopodia formation and associated ECM degradation activity.",
author = "Hwang, {Young Sun} and Park, {Kwang Kyun} and WonYoon Chung",
year = "2012",
month = "4",
day = "1",
doi = "10.1016/j.archoralbio.2011.08.019",
language = "English",
volume = "57",
pages = "335--343",
journal = "Archives of Oral Biology",
issn = "0003-9969",
publisher = "Elsevier Limited",
number = "4",

}

Invadopodia formation in oral squamous cell carcinoma : The role of epidermal growth factor receptor signalling. / Hwang, Young Sun; Park, Kwang Kyun; Chung, WonYoon.

In: Archives of Oral Biology, Vol. 57, No. 4, 01.04.2012, p. 335-343.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Invadopodia formation in oral squamous cell carcinoma

T2 - The role of epidermal growth factor receptor signalling

AU - Hwang, Young Sun

AU - Park, Kwang Kyun

AU - Chung, WonYoon

PY - 2012/4/1

Y1 - 2012/4/1

N2 - Objective: Invadopodia are actin-rich structures that are formed on the ventral membrane of the cell and degrade extracellular matrix (ECM) by accumulation of matrix metalloproteinase (MMP). Consequently, understanding how invadopodia form and function should facilitate the identification of new therapeutic target for anti-invadopodia therapy. The present study was designed to investigate invadopodia formation associated with oral squamous cell carcinoma (OSCC) and the effect of epidermal growth factor receptor (EGFR) signalling on invadopodia formation and ECM degradation activity. Design: Immunofluorescence analysis of invadopodia formation and ECM degradation was performed using confocal microscope. To understand the role of EGFR signalling, cells were treated with AG1478 or PD153035 (EGF receptor tyrosine kinase inhibitors) and assessed using zymography and an ECM degradation assay. Results: Invadopodia containing dot-shaped F-actin were observed in stress fibres of HSC-3 OSCC along with evidence of ECM degradation activity. GM6001, a broad range of MMP inhibitor impaired matrix degradation and gelatinolytic activity of active MMP-2. AG1478 and PD153035 inhibited invadopodia formation and ECM degradation activity, as well as gelatinolytic activity of proMMP-9 and proMMP-2. Conclusions: We provide evidence that HSC-3 OSCC has a tendency to adopt invadopodia for invasion and accompanying MMP-dependent proteolytic ECM degradation and EGFR signalling is necessary for invadopodia formation and associated ECM degradation activity.

AB - Objective: Invadopodia are actin-rich structures that are formed on the ventral membrane of the cell and degrade extracellular matrix (ECM) by accumulation of matrix metalloproteinase (MMP). Consequently, understanding how invadopodia form and function should facilitate the identification of new therapeutic target for anti-invadopodia therapy. The present study was designed to investigate invadopodia formation associated with oral squamous cell carcinoma (OSCC) and the effect of epidermal growth factor receptor (EGFR) signalling on invadopodia formation and ECM degradation activity. Design: Immunofluorescence analysis of invadopodia formation and ECM degradation was performed using confocal microscope. To understand the role of EGFR signalling, cells were treated with AG1478 or PD153035 (EGF receptor tyrosine kinase inhibitors) and assessed using zymography and an ECM degradation assay. Results: Invadopodia containing dot-shaped F-actin were observed in stress fibres of HSC-3 OSCC along with evidence of ECM degradation activity. GM6001, a broad range of MMP inhibitor impaired matrix degradation and gelatinolytic activity of active MMP-2. AG1478 and PD153035 inhibited invadopodia formation and ECM degradation activity, as well as gelatinolytic activity of proMMP-9 and proMMP-2. Conclusions: We provide evidence that HSC-3 OSCC has a tendency to adopt invadopodia for invasion and accompanying MMP-dependent proteolytic ECM degradation and EGFR signalling is necessary for invadopodia formation and associated ECM degradation activity.

UR - http://www.scopus.com/inward/record.url?scp=84858707888&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84858707888&partnerID=8YFLogxK

U2 - 10.1016/j.archoralbio.2011.08.019

DO - 10.1016/j.archoralbio.2011.08.019

M3 - Article

VL - 57

SP - 335

EP - 343

JO - Archives of Oral Biology

JF - Archives of Oral Biology

SN - 0003-9969

IS - 4

ER -