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. 2019 Dec 30;12(1):97. doi: 10.3390/cancers12010097

Figure 3.

Figure 3

c-Jun N-terminal kinase (JNK) activation participated in TAX- and NOC-induced apoptosis of human CRC cells. (A) The JNK inhibitor SP600125 (SP) protected cells from TAX- and NOC-induced cytotoxicity in human CRC cells. Human CRC cells were treated with SP (10 μM) for 30 min followed by TAX or NOC (10 µM) treatment for 24 h. The viability of cells under different treatments was examined by an MTT assay, and results are expressed as a percentage of the control (% of CON). (B) SP inhibition of cleavage of Casp-3 protein in human CRC cells. As described in (A), expressions of the Casp-3 and α-TUB proteins were examined by Western blotting using specific antibodies. (C) Addition of JNK inhibitor V (JNKI) reversed the cytotoxicity of TAX and NOC in HCT-15, HT-29, and COLO205 cells. Cells were treated with JNKI (10 μM) for 30 min followed by TAX and NOC (10 μM) treatment for 24 h. The viability of the cells was examined by an MTT assay. (D) SP and JNKI inhibited TAX- and NOC-induced DNA ladders in human CRC cells. As described above, DNA integrity was examined by agarose electrophoresis. Data from three independent experiments were obtained and are displayed as the mean ± SD. ** p < 0.01 denotes a significant difference between indicated groups.