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. 2007 Oct 19;99(1):129–139. doi: 10.1111/j.1349-7006.2007.00637.x

Figure 6.

Figure 6

Oxaliplatin (OHP)‐induced apoptosis. (a) Annexin V apoptosis assay. Following 24‐h treatment with OHP (2.5 µM for both) and cisplatin (CDDP; 2.5 µM for TE3, 3 µM for TE7) treatment, cells were labeled with annexin V–fluorescein isothiocyanate antibody and detected using flow cytometry. Positive cells were predominantly in early apoptosis. With OHP treatment, an increase in apoptotic cells was detected in the TE3 cell line, but was limited in TE7 cells. CDDP induced apoptosis to a lesser extent in TE3 cells but a higher extent in TE7 compared with OHP treatment. Statistical significance is indicated by the P‐value. (b) Western blotting analysis of polyADP‐ribose polymerase (PARP) cleavage confirmed that apoptosis was occurring in TE3 cells after OHP treatment (an increase in the fraction of cleaved PARP), whereas PARP remained uncleaved in TE7 cells until 72 h. (c) Caspase expression. Cleaved caspase‐3 was evident at 72 h in TE3 cells. Actin was included as a loading control. (d) Apoptosis assessed by annexin V assay with flow cytometry. Caspase‐3 (z‐DEVD‐fmk), caspase‐9 (z‐LEHD‐fmk), and pan‐caspase (z‐VAD‐fmk) inhibitors significantly blocked OHP‐induced apoptosis in TE3 cells.