机构：[1]Department of Mammary Disease, Guangdong Provincial Hospital of Chinese Medicine, The Second Clinical Collage of Guangzhou University of Chinese Medicine, Guangzhou, China大德路总院乳腺科大德路总院乳腺科广东省中医院[2]Department of Breast Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China
This chapter focuses on the role of AMPK as a stress-response molecule with an emphasis on its duplex implication in carcinogenesis and cancer drug resistance. AMPK is closely correlated to the tumor-suppressive functions of LKB1 and P53, consequently modulating the activity of cellular survival signaling such as mTOR and Akt, leading to cell growth inhibition and cell cycle arrest. On the contrary, AMPK is tightly involved in cancer drug resistance via interacting with multiple known mechanisms of chemoresistance such as ABCG2 expression, autophagy induction, and cancer stem cells enrichment. Targeting AMPK has become a novel strategy for cancer prevention and treatment.
基金：
This work was supported by the National Natural Science Foundation of
China (81402173 and 81573651) and Pearl River S&T Nova Program of Guangzhou
(201506010098).
语种：
外文
WOS：
PubmedID：
第一作者：
第一作者机构：[1]Department of Mammary Disease, Guangdong Provincial Hospital of Chinese Medicine, The Second Clinical Collage of Guangzhou University of Chinese Medicine, Guangzhou, China
通讯作者：
推荐引用方式(GB/T 7714)：
Wang Zhiyu,Wang Neng,Liu Pengxi,et al.AMPK and Cancer.[J].AMP-ACTIVATED PROTEIN KINASE.2016,107:203-226.doi:10.1007/978-3-319-43589-3_9.
APA：
Wang Zhiyu,Wang Neng,Liu Pengxi&Xie Xiaoming.(2016).AMPK and Cancer..AMP-ACTIVATED PROTEIN KINASE,107,
MLA：
Wang Zhiyu,et al."AMPK and Cancer.".AMP-ACTIVATED PROTEIN KINASE 107.(2016):203-226
