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Binding of TGF-beta1 latency-associated peptide (LAP) to alpha(v)beta6 integrin modulates behaviour of squamous carcinoma cells.

Thomas GJ, Hart IR, Speight PM, Marshall JF - Br. J. Cancer (2002)

Bottom Line: Since TGF-beta1 is present in squamous carcinomas, it is possible that latency associated peptide may modulate malignant keratinocyte behaviour independently from the classical TGF-beta signalling pathways through its interaction with integrins.We show here that when latency associated peptide is immobilised onto a surface, it acts as an alpha(v)beta6-specific ligand for oral squamous carcinoma cells promoting adhesion and haptotactic migration in addition to alpha(v)beta6-dependent increase in pro-MMP-9 expression.In contrast, even very low concentrations of soluble latency associated peptide (0.1 microg ml(-1)) inhibited alpha(v)beta6-dependent adhesion, migration and invasion.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral Pathology, Eastman Dental Institute, University College London, UK.

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Cell adhesion to LAP is αvβ6-dependent. Chromium [51Cr]- labelled cells (1.5×104) were added to LAP-coated 96-well plates containing an irrelevant control antibody (W632 anti-MHC class 1) or test antibodies against αv (L230), αvβ5 (P1F6), αvβ6 (10D5), β1 (P4C10) and α5β1 (P1D6). Background binding to BSA has been subtracted from the results. Figures show representative experiments performed in quadruplicate. Error bars represent standard deviation. (A) VB6 cells show increased adherence LAP. β6 transfected cells (VB6), control cells (C1) and αv-negative cells (H357) were plated onto varying concentrations of LAP. VB6 cells showed significantly increased adhesion compared to C1 cells (which express low levels of endogenous αvβ6). H357 cells did not adhere. (B) Adhesion to LAP is αvβ6-dependent. VB6 and C1 adhesion to LAP was inhibited by anti-αvβ6 antibody or anti-αv antibody. Antibodies against αvβ5, α5β1 or β1 produced no effect. These data suggest that adhesion of VB6 and C1 cells is modulated solely through αvβ6.
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fig2: Cell adhesion to LAP is αvβ6-dependent. Chromium [51Cr]- labelled cells (1.5×104) were added to LAP-coated 96-well plates containing an irrelevant control antibody (W632 anti-MHC class 1) or test antibodies against αv (L230), αvβ5 (P1F6), αvβ6 (10D5), β1 (P4C10) and α5β1 (P1D6). Background binding to BSA has been subtracted from the results. Figures show representative experiments performed in quadruplicate. Error bars represent standard deviation. (A) VB6 cells show increased adherence LAP. β6 transfected cells (VB6), control cells (C1) and αv-negative cells (H357) were plated onto varying concentrations of LAP. VB6 cells showed significantly increased adhesion compared to C1 cells (which express low levels of endogenous αvβ6). H357 cells did not adhere. (B) Adhesion to LAP is αvβ6-dependent. VB6 and C1 adhesion to LAP was inhibited by anti-αvβ6 antibody or anti-αv antibody. Antibodies against αvβ5, α5β1 or β1 produced no effect. These data suggest that adhesion of VB6 and C1 cells is modulated solely through αvβ6.

Mentions: Preliminary studies indicated that optimal adhesion to LAP was achieved at a concentration of 0.25 μg ml−1 (Figure 2AFigure 2


Binding of TGF-beta1 latency-associated peptide (LAP) to alpha(v)beta6 integrin modulates behaviour of squamous carcinoma cells.

Thomas GJ, Hart IR, Speight PM, Marshall JF - Br. J. Cancer (2002)

Cell adhesion to LAP is αvβ6-dependent. Chromium [51Cr]- labelled cells (1.5×104) were added to LAP-coated 96-well plates containing an irrelevant control antibody (W632 anti-MHC class 1) or test antibodies against αv (L230), αvβ5 (P1F6), αvβ6 (10D5), β1 (P4C10) and α5β1 (P1D6). Background binding to BSA has been subtracted from the results. Figures show representative experiments performed in quadruplicate. Error bars represent standard deviation. (A) VB6 cells show increased adherence LAP. β6 transfected cells (VB6), control cells (C1) and αv-negative cells (H357) were plated onto varying concentrations of LAP. VB6 cells showed significantly increased adhesion compared to C1 cells (which express low levels of endogenous αvβ6). H357 cells did not adhere. (B) Adhesion to LAP is αvβ6-dependent. VB6 and C1 adhesion to LAP was inhibited by anti-αvβ6 antibody or anti-αv antibody. Antibodies against αvβ5, α5β1 or β1 produced no effect. These data suggest that adhesion of VB6 and C1 cells is modulated solely through αvβ6.
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Related In: Results  -  Collection

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fig2: Cell adhesion to LAP is αvβ6-dependent. Chromium [51Cr]- labelled cells (1.5×104) were added to LAP-coated 96-well plates containing an irrelevant control antibody (W632 anti-MHC class 1) or test antibodies against αv (L230), αvβ5 (P1F6), αvβ6 (10D5), β1 (P4C10) and α5β1 (P1D6). Background binding to BSA has been subtracted from the results. Figures show representative experiments performed in quadruplicate. Error bars represent standard deviation. (A) VB6 cells show increased adherence LAP. β6 transfected cells (VB6), control cells (C1) and αv-negative cells (H357) were plated onto varying concentrations of LAP. VB6 cells showed significantly increased adhesion compared to C1 cells (which express low levels of endogenous αvβ6). H357 cells did not adhere. (B) Adhesion to LAP is αvβ6-dependent. VB6 and C1 adhesion to LAP was inhibited by anti-αvβ6 antibody or anti-αv antibody. Antibodies against αvβ5, α5β1 or β1 produced no effect. These data suggest that adhesion of VB6 and C1 cells is modulated solely through αvβ6.
Mentions: Preliminary studies indicated that optimal adhesion to LAP was achieved at a concentration of 0.25 μg ml−1 (Figure 2AFigure 2

Bottom Line: Since TGF-beta1 is present in squamous carcinomas, it is possible that latency associated peptide may modulate malignant keratinocyte behaviour independently from the classical TGF-beta signalling pathways through its interaction with integrins.We show here that when latency associated peptide is immobilised onto a surface, it acts as an alpha(v)beta6-specific ligand for oral squamous carcinoma cells promoting adhesion and haptotactic migration in addition to alpha(v)beta6-dependent increase in pro-MMP-9 expression.In contrast, even very low concentrations of soluble latency associated peptide (0.1 microg ml(-1)) inhibited alpha(v)beta6-dependent adhesion, migration and invasion.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral Pathology, Eastman Dental Institute, University College London, UK.

Show MeSH
Related in: MedlinePlus