Kinetin riboside preferentially induces apoptosis by modulating Bcl-2 family proteins and caspase-3 in cancer cells

• Main Authors: Choi, Bo-Hwa, Kim, Wanil, Wang, Qiuxia Chelsia, Kim, Dong-Chan, Tan, Swee Ngin, Yong, Jean Wan Hong, Kim, Kyong-Tai, Yoon, Ho Sup
• Other Authors: School of Biological Sciences
• Format: Article
• Language: English
• Published: 2012
• Subjects: DRNTU::Science::Biological sciences
• Online Access: https://hdl.handle.net/10356/99906; http://hdl.handle.net/10220/8384
• Institution: Nanyang Technological University

Here, we demonstrate that kinetin riboside (KR), a cytokinin analog, induces apoptosis in HeLa and mouse melanoma B16F-10 cells. KR disrupted the mitochondrial membrane potential and induced the release of cytochrome c and activation of caspase-3. Bad were upregulated while Bcl-2 was down-regulated under KR exposure. A tumor growth in mice was dramatically suppressed by KR. In contrast, human skin fibroblast CCL-116 and bovine primary fibroblast cells show resistances to KR and no significant changes in Bad, Bcl-XL, and cleaved PARP were observed. Our data suggest that KR selectively induces apoptosis in cancer cells through the classical mitochondria dependent apoptosis pathway.