. Author manuscript; available in PMC: 2012 Jul 12.

Published in final edited form as: Oncogene. 2011 Jun 20;31(2):149–160. doi: 10.1038/onc.2011.222

Table 1B.

Effects of an IAP inhibitor (SM-164) on cisplatin-induced apoptosis and cell growth inhibition in HSC-3 cells

Treatments	Apoptotic Cells (Annexin V-positive cell/total cells x 100%)^*		Cisplatin-Induced Tumor Cell Growth Inhibition IC₅₀ (μM)^**
Treatments	No Cisplatin	+ Cisplatin	Cisplatin-Induced Tumor Cell Growth Inhibition IC₅₀ (μM)^**
Vehicle control-treated cells (No HA)	13 ± 2	42 ± 4	1.0
Vehicle control-treated cells (+ HA)	6 ± 3	14 ± 4	35.00
SM-164-treated cells (no HA)	27 ± 6	87 ± 6	0.05
SM-164-trerated cells (+ HA)	12 ± 4	68 ± 9	0.10

Cells were designated apoptotic when displaying Annexin V-positive staining. In each sample, at least 500 cells from five different fields were counted, with the percentage of cisplatin (2h treatment)-induced apoptotic cells calculated as Annexin V-positive cells/total number of cells. The values are presented as the means±standard deviation. All assays consisted of at least six replicates and were performed on at least 3–5 different experiments.

^**

Tumor cell growth inhibition (IC₅₀) is designated as “the μM concentration of chemotherapeutic drug (e.g., cisplatin-24h treatment) that causes 50% inhibition of tumor cell growth” using MTT-based growth assay as described in the Materials and Methods. IC₅₀ values are presented as the means±standard deviation. All assays consisted of at least six replicates and were performed on at least 3–5 different experiments.