Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion

Chondrosarcoma develops as a result of overgrowth of chondrocytes and overproduction of cartilage matrix. It is currently surgically treated, although non-invasive methods are being sought. In this report, pigment epithelium-derived factor (PEDF) induced apoptosis in the chondrosarcoma cell line - J...

Full description

Bibliographic Details
Main Authors: Tan, M., Choong, P., Dass, Crispin
Format: Journal Article
Published: Academic Press 2010
Online Access:http://hdl.handle.net/20.500.11937/14830
_version_ 1848748727884316672
author Tan, M.
Choong, P.
Dass, Crispin
author_facet Tan, M.
Choong, P.
Dass, Crispin
author_sort Tan, M.
building Curtin Institutional Repository
collection Online Access
description Chondrosarcoma develops as a result of overgrowth of chondrocytes and overproduction of cartilage matrix. It is currently surgically treated, although non-invasive methods are being sought. In this report, pigment epithelium-derived factor (PEDF) induced apoptosis in the chondrosarcoma cell line - JJ012, with upregulation of Bax, Fas, caspase-3 and -6 and downregulation of Bcl-2. Cell cycling was also decreased with decreased expression of p38, p-Akt, p-Erk and JNK1 and increased expression of p73 and E2F1. Furthermore, PEDF increased adhesion of cells to collagen-I, with decreased expression of p-Fak, RhoA and cdc42. Invasion of cells through collagen-I was also reduced by PEDF, with decreased expression of uPAR, MMP-14 and increased expression of PAI-1. These findings seminally indicate that PEDF may have potential as an anti-cancer agent against chondrosarcoma.
first_indexed 2025-11-14T07:09:39Z
format Journal Article
id curtin-20.500.11937-14830
institution Curtin University Malaysia
institution_category Local University
last_indexed 2025-11-14T07:09:39Z
publishDate 2010
publisher Academic Press
recordtype eprints
repository_type Digital Repository
spelling curtin-20.500.11937-148302017-09-13T14:06:27Z Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion Tan, M. Choong, P. Dass, Crispin Chondrosarcoma develops as a result of overgrowth of chondrocytes and overproduction of cartilage matrix. It is currently surgically treated, although non-invasive methods are being sought. In this report, pigment epithelium-derived factor (PEDF) induced apoptosis in the chondrosarcoma cell line - JJ012, with upregulation of Bax, Fas, caspase-3 and -6 and downregulation of Bcl-2. Cell cycling was also decreased with decreased expression of p38, p-Akt, p-Erk and JNK1 and increased expression of p73 and E2F1. Furthermore, PEDF increased adhesion of cells to collagen-I, with decreased expression of p-Fak, RhoA and cdc42. Invasion of cells through collagen-I was also reduced by PEDF, with decreased expression of uPAR, MMP-14 and increased expression of PAI-1. These findings seminally indicate that PEDF may have potential as an anti-cancer agent against chondrosarcoma. 2010 Journal Article http://hdl.handle.net/20.500.11937/14830 10.1016/j.bbrc.2010.05.098 Academic Press restricted
spellingShingle Tan, M.
Choong, P.
Dass, Crispin
Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
title Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
title_full Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
title_fullStr Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
title_full_unstemmed Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
title_short Anti-chondrosarcoma effects of PEDF mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
title_sort anti-chondrosarcoma effects of pedf mediated via molecules important to apoptosis, cell cycling, adhesion and invasion
url http://hdl.handle.net/20.500.11937/14830