ATM and LKB1 dependent activation of AMPK sensitizes cancer cells to etoposide-induced apoptosis |
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| Authors: | Lingyu Luo Wei Huang Rong Tao Ningyan Hu Zhi-Xiong Xiao Zhijun Luo |
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| Affiliation: | 1. Research Institute of Digestive Diseases, The First Hospital, Nanchang University, Nanchang, Jiangxi, China;2. Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA;3. Department of Biochemistry, Guangzhou Medical College, Guangzhou, Guangdong, China;4. School of Basic Medical Sciences, Nanchang University College of Medicine, Nanchang, Jiangxi, China;5. College of Life Science, Sichuan University, Chengdu, China |
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| Abstract: | The present study aims to determine the effect of AMPK on etoposide-induced apoptosis of cancer cells. Our results revealed that etoposide induced AMPK activation in prostate C4-2 cancer cells, an event that was attenuated by ATM siRNA. In A549 cells that lack LKB1, AMPK was unable to be activated by etoposide, which was restored by introduction of LKB1. Likewise, silencing LKB1 in C4-2 cells impaired AMPK activation. Finally, etoposide displayed a potent pro-apoptotic effect in cancer cells with functional LKB1 and AMPK. Thus, our results establish a linear relationship of ATM, LKB1 and AMPK in response to the DNA damage drug. |
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