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CD26 Expression on T-Anaplastic Large Cell Lymphoma (ALCL) Line Karpas 299 is associated with increased expression of Ve...

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Title:
CD26 Expression on T-Anaplastic Large Cell Lymphoma (ALCL) Line Karpas 299 is associated with increased expression of Versican and MT1-MMP and enhanced adhesion
Physical Description:
Mixed Material
Language:
English
Creator:
Havre, Pamela A.
Dang, Long H.
Ohnuma, Kei
Iwata, Satoshi
Morimoto, Chikao
Dang, Nam H.
Publisher:
Bio-Med Central (BMC Cancer)
Publication Date:

Notes

Abstract:
Background: CD26/dipeptidyl peptidase IV (DPPIV) is a multifunctional membrane protein with a key role in T-cell biology and also serves as a marker of aggressive cancers, including T-cell malignancies. Methods: Versican expression was measured by real-time RT-PCR and Western blots. Gene silencing of versican in parental Karpas 299 cells was performed using transduction-ready viral particles. The effect of versican depletion on surface expression of MT1-MMP was monitored by flow cytometry and surface biotinylation. CD44 secretion/ cleavage and ERK (1/2) activation was followed by Western blotting. Collagenase I activity was measured by a live cell assay and in vesicles using a liquid-phase assay. Adhesion to collagen I was quantified by an MTS assay. Results: Versican expression was down-regulated in CD26-depleted Karpas 299 cells compared to the parental T-ALCL Karpas 299 cells. Knock down of versican in the parental Karpas 299 cells led to decreased MT1-MMP surface expression as well as decreased CD44 expression and secretion of the cleaved form of CD44. Parental Karpas 299 cells also exhibited higher collagenase I activity and greater adhesion to collagenase I than CD26-knockdown or versican-knockdown cells. ERK activation was also highest in parental Karpas 299 cells compared to CD26-knockdown or versican-knockdown clones. Conclusions: Our data indicate that CD26 has a key role in cell adhesion and invasion, and potentially in tumorigenesis of T-cell lines, through its association with molecules and signal transduction pathways integral to these processes. Keywords: CD26, T-cell malignancies, Adhesion, MT1-MMP, Cell signaling
General Note:
Havre et al. BMC Cancer 2013, 13:517 http://www.biomedcentral.com/1471-2407/13/517; Pages 1-11
General Note:
doi:10.1186/1471-2407-13-517 Cite this article as: Havre et al.: CD26 Expression on T-Anaplastic Large Cell Lymphoma (ALCL) Line Karpas 299 is associated with increased expression of Versican and MT1-MMP and enhanced adhesion. BMC Cancer 2013 13:517.

Record Information

Source Institution:
University of Florida
Holding Location:
University of Florida
Rights Management:
All rights reserved by the source institution.
Resource Identifier:
oclc -
System ID:
AA00019188:00001

  • STANDARD VIEW
  • MARC VIEW

Material Information

Title:
CD26 Expression on T-Anaplastic Large Cell Lymphoma (ALCL) Line Karpas 299 is associated with increased expression of Versican and MT1-MMP and enhanced adhesion
Physical Description:
Mixed Material
Language:
English
Creator:
Havre, Pamela A.
Dang, Long H.
Ohnuma, Kei
Iwata, Satoshi
Morimoto, Chikao
Dang, Nam H.
Publisher:
Bio-Med Central (BMC Cancer)
Publication Date:

Notes

Abstract:
Background: CD26/dipeptidyl peptidase IV (DPPIV) is a multifunctional membrane protein with a key role in T-cell biology and also serves as a marker of aggressive cancers, including T-cell malignancies. Methods: Versican expression was measured by real-time RT-PCR and Western blots. Gene silencing of versican in parental Karpas 299 cells was performed using transduction-ready viral particles. The effect of versican depletion on surface expression of MT1-MMP was monitored by flow cytometry and surface biotinylation. CD44 secretion/ cleavage and ERK (1/2) activation was followed by Western blotting. Collagenase I activity was measured by a live cell assay and in vesicles using a liquid-phase assay. Adhesion to collagen I was quantified by an MTS assay. Results: Versican expression was down-regulated in CD26-depleted Karpas 299 cells compared to the parental T-ALCL Karpas 299 cells. Knock down of versican in the parental Karpas 299 cells led to decreased MT1-MMP surface expression as well as decreased CD44 expression and secretion of the cleaved form of CD44. Parental Karpas 299 cells also exhibited higher collagenase I activity and greater adhesion to collagenase I than CD26-knockdown or versican-knockdown cells. ERK activation was also highest in parental Karpas 299 cells compared to CD26-knockdown or versican-knockdown clones. Conclusions: Our data indicate that CD26 has a key role in cell adhesion and invasion, and potentially in tumorigenesis of T-cell lines, through its association with molecules and signal transduction pathways integral to these processes. Keywords: CD26, T-cell malignancies, Adhesion, MT1-MMP, Cell signaling
General Note:
Havre et al. BMC Cancer 2013, 13:517 http://www.biomedcentral.com/1471-2407/13/517; Pages 1-11
General Note:
doi:10.1186/1471-2407-13-517 Cite this article as: Havre et al.: CD26 Expression on T-Anaplastic Large Cell Lymphoma (ALCL) Line Karpas 299 is associated with increased expression of Versican and MT1-MMP and enhanced adhesion. BMC Cancer 2013 13:517.

Record Information

Source Institution:
University of Florida
Holding Location:
University of Florida
Rights Management:
All rights reserved by the source institution.
Resource Identifier:
oclc -
System ID:
AA00019188:00001