Article

Effects of anti-EGFR antibody cetuximab on androgen-independent prostate cancer cells.

Department of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences in Philadelphia, 600 South 43rd Street, Philadelphia, PA 19104, USA.
Anticancer research (impact factor: 1.73). 06/2010; 30(6):1905-10. pp.1905-10
Source: PubMed

ABSTRACT Epidermal growth factor receptor (EGFR) is a novel molecular target for anticancer therapy. This study examined the effects of anti-EGFR antibody cetuximab on two human androgen-independent prostate carcinoma cell lines, Du145 and PC-3.
Cell proliferation was monitored with a trypan blue viability assay. Cell apoptosis and cell cycle profile was evaluated by flow cytometry. The expression of various signaling molecules was examined by Western immunoblotting.
Cetuximab (100 microg/ml) caused a significant growth inhibition by inducing cell apoptosis in Du145 cells, but not in PC-3 cells. It caused EGFR down-regulation and inhibited EGFR Tyr-845 autophosphorylation in both Du145 and PC-3 cells. However, EGFR phosphorylation at Tyr-1173 and MAPK 44/42 phosphorylation were inhibited in Du145 cells, but not in PC-3 cells. Cetuximab was not able to inhibit Akt phosphorylation in either prostate cancer cell line.
Du145 cells only showed a very moderate response to cetuximab whereas PC-3 cells showed resistance. Persistent activation of EGFR downstream signaling likely contributes to cell resistance to cetuximab.

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    BMC Cancer 08/2011; 11:375. · 3.01 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

Akt phosphorylation
 
anti-EGFR antibody cetuximab
 
anticancer therapy
 
cell cycle profile
 
Cetuximab
 
EGFR
 
EGFR down-regulation
 
EGFR downstream signaling likely contributes
 
EGFR phosphorylation
 
Epidermal growth factor receptor
 
human androgen-independent prostate carcinoma cell lines
 
inhibited EGFR Tyr-845 autophosphorylation
 
MAPK 44/42 phosphorylation
 
PC-3
 
PC-3 cells
 
prostate cancer cell line
 
trypan blue viability assay
 
Western immunoblotting