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. Author manuscript; available in PMC: 2011 Feb 2.
Published in final edited form as: Clin Cancer Res. 2008 Sep 1;14(17):5341–5347. doi: 10.1158/1078-0432.CCR-08-0793

Fig. 3.

Fig. 3

β2M antibody induced the cell death of prostate cancer cells through an apoptotic cascade pathway. A, LNCaP and C4-2B cells were exposed to either the β2M antibody or isotype control IgG (10 μg/mL) for 48-h incubation and subjected to cell cycle analysis determined by flow cytometry. Both LNCaP and C4-2B cells treated with the β2M antibody showed a marked increase in the sub-G1DNA contents compared with IgG-treated cells. B, β2M antibody (0-10 μg/mL, 48-h treatment) activated the expression of cleaved caspase-9, caspase-3, and PARP proteins in a dose-dependent pattern in LNCaP and C4-2B cells as assayed by Western blot. β2M protein rescued the apoptotic effect of the β2M antibody. Control IgG (10 μg/mL) did not activate cleaved caspase and PARP expression. C, LNCaP and C4-2B cells were treated with the β2M antibody; the β2M antibody was preincubated with β2M protein or control IgG (10 μg/mL) for 48 h and examined by light microscopy. Bar, 250 μm.