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

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-regu...

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Bibliographic Details
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:
Online Access:https://hdl.handle.net/10356/99906
http://hdl.handle.net/10220/8384
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Institution: Nanyang Technological University
Language: English
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Summary: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.