title: Unravelling the relationship between macroautophagy and mitochondrial ROS in cancer therapy.
abstract: Macroautophagy (Autophagy), an evolutionarily conserved cellular self-digesting process implicated in various physiological and pathological processes, is activated by different stimuli including oxidative stress. Reactive oxygen species (ROS) are involved in autophagy modulation through multiple signaling pathways and transcription regulators. Accumulating data support both a positive and negative role of ROS-modulated autophagy in cancer. As a tumor suppressive mechanism, autophagy induces autophagic cell death and maintains genome stability. Conversely, autophagy may promote cancer development by limiting metabolic stress and supplying high-energetic nutrients. Mitochondrial ROS (mitoROS), the main source of endogenous ROS, serve as essential signal transducers that mediate autophagy, while autophagy can also regulate mitochondrial ROS generation in turn. Here, we untangle the knot between mitochondrial ROS and autophagy, which may be of great significance to solve the conundrum of the inter-conversion between cytoprotective and cytotoxic roles of autophagy; thus providing new insights for current cancer therapies. Whilst, we focus on anti-tumor agents that target mitoROS-regulated autophagy, in the hope of fueling the exploration of more potential novel anti-cancer drugs in the future.
authors.affiliation: Key Laboratory of Structure-Based Drug Design & Discovery of Ministry of Education, School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, 110016, China.
authors.forename: Yuqian
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: School of Basic Medicine Science, Beijing University of Chinese Medicine, Beijing, 100029, China.
authors.forename: Tiange
authors.initials: T
authors.lastname: Qu
authors.affiliation: State Key Laboratory of Stomatology, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
authors.forename: Peiqi
authors.initials: P
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Stomatology, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China.
authors.forename: Xinyi
authors.initials: X
authors.lastname: Li
authors.affiliation: College of Life Sciences, Sichuan University, Chengdu, 610064, China.
authors.forename: Jiayu
authors.initials: J
authors.lastname: Qiang
authors.affiliation: College of Life Sciences, Sichuan University, Chengdu, 610064, China.
authors.forename: Zhaokun
authors.initials: Z
authors.lastname: Xia
authors.affiliation: School of Basic Medicine Science, Beijing University of Chinese Medicine, Beijing, 100029, China.
authors.forename: Hangwu
authors.initials: H
authors.lastname: Duan
authors.affiliation: Key Laboratory of Structure-Based Drug Design & Discovery of Ministry of Education, School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, 110016, China. profhj@163.com.
authors.forename: Jian
authors.initials: J
authors.lastname: Huang
authors.affiliation: Key Laboratory of Structure-Based Drug Design & Discovery of Ministry of Education, School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, 110016, China. zhulingjuanadele@163.com.
authors.forename: Lingjuan
authors.initials: L
authors.lastname: Zhu
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001343:Autophagy / Q000187:drug effects; D063646:Carcinogenesis; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009369:Neoplasms / Q000188:drug therapy / Q000209:etiology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D000970:Antineoplastic Agents; D017382:Reactive Oxygen Species
keywords: Autophagy; Cancer therapy; Macroautophagy; Mitochondrial ROS (mitoROS); Reactive oxygen species (ROS)