Reactive oxygen species in cancer: Current findings and future directions

被引:607
作者
Nakamura, Hajime [1 ]
Takada, Kohichi [1 ]
机构
[1] Sapporo Med Univ, Sch Med, Dept Med Oncol, Sapporo, Hokkaido, Japan
基金
日本学术振兴会;
关键词
cell death; neoplasms; oxidative stress; reactive oxygen species; therapeutics; REGULATORY T-CELLS; OXIDATIVE STRESS; MITOCHONDRIAL ROS; P-GLYCOPROTEIN; DNA; AUTOPHAGY; RESISTANCE; APOPTOSIS; DAMAGE; IRON;
D O I
10.1111/cas.15068
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Reactive oxygen species (ROS), a class of highly bioactive molecules, have been widely studied in various types of cancers. ROS are considered to be normal byproducts of numerous cellular processes. Typically, cancer cells exhibit higher basal levels of ROS compared with normal cells as a result of an imbalance between oxidants and antioxidants. ROS have a dual role in cell metabolism: At low to moderate levels, ROS act as signal transducers to activate cell proliferation, migration, invasion, and angiogenesis. In contrast, high levels of ROS cause damage to proteins, nucleic acids, lipids, membranes, and organelles, leading to cell death. Extensive studies have revealed that anticancer therapies that manipulate ROS levels, including immunotherapies, show promising in vitro as well as in vivo results. In this review, we summarize molecular mechanisms and oncogenic functions that modulate ROS levels and are useful for the development of cancer therapeutic strategies. This review also provides insights into the future development of effective agents that regulate the redox system for cancer treatment.
引用
收藏
页码:3945 / 3952
页数:8
相关论文
共 70 条
[1]   P-glycoprotein: from genomics to mechanism [J].
Ambudkar, SV ;
Kimchi-Sarfaty, C ;
Sauna, ZE ;
Gottesman, MM .
ONCOGENE, 2003, 22 (47) :7468-7485
[2]   Iron Chelation in Transfusion-Dependent Patients With Low- to Intermediate-1-Risk Myelodysplastic Syndromes A Randomized Trial [J].
Angelucci, Emanuele ;
Li, Junmin ;
Greenberg, Peter ;
Wu, Depei ;
Hou, Ming ;
Montano Figueroa, Efreen Horacio ;
Guadalupe Rodriguez, Maria ;
Dong, Xunwei ;
Ghosh, Jagannath ;
Izquierdo, Miguel ;
Garcia-Manero, Guillermo .
ANNALS OF INTERNAL MEDICINE, 2020, 172 (08) :513-+
[3]   Small molecule CP-31398 induces reactive oxygen species-dependent apoptosis in human multiple myeloma [J].
Arihara, Yohei ;
Takada, Kohichi ;
Kamihara, Yusuke ;
Hayasaka, Naotaka ;
Nakamura, Hajime ;
Murase, Kazuyuki ;
Ikeda, Hiroshi ;
Iyama, Satoshi ;
Sato, Tsutomu ;
Miyanishi, Koji ;
Kobune, Masayoshi ;
Kato, Junji .
ONCOTARGET, 2017, 8 (39) :65889-65899
[4]   Mitochondria, oxidants, and aging [J].
Balaban, RS ;
Nemoto, S ;
Finkel, T .
CELL, 2005, 120 (04) :483-495
[5]   Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms [J].
Beyersmann, Detmar ;
Hartwig, Andrea .
ARCHIVES OF TOXICOLOGY, 2008, 82 (08) :493-512
[6]   OXIDATIVE STRESS: AN ESSENTIAL FACTOR IN THE PATHOGENESIS OF GASTROINTESTINAL MUCOSAL DISEASES [J].
Bhattacharyya, Asima ;
Chattopadhyay, Ranajoy ;
Mitra, Sankar ;
Crowe, Sheila E. .
PHYSIOLOGICAL REVIEWS, 2014, 94 (02) :329-354
[7]   Iron and Reactive Oxygen Species: Friends or Foes of Cancer Cells? [J].
Bystrom, Laura M. ;
Guzman, Monica L. ;
Rivella, Stefano .
ANTIOXIDANTS & REDOX SIGNALING, 2014, 20 (12) :1917-1924
[8]   Regulation of cancer cell metabolism [J].
Cairns, Rob A. ;
Harris, Isaac S. ;
Mak, Tak W. .
NATURE REVIEWS CANCER, 2011, 11 (02) :85-95
[9]   Mitochondrial activation chemicals synergize with surface receptor PD-1 blockade for T cell-dependent antitumor activity [J].
Chamoto, Kenji ;
Chowdhury, Partha S. ;
Kumar, Alok ;
Sonomura, Kazuhiro ;
Matsuda, Fumihiko ;
Fagarasan, Sidonia ;
Honjo, Tasuku .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2017, 114 (05) :E761-E770
[10]   ROS in Cancer: The Burning Question [J].
Chio, Iok In Christine ;
Tuveson, David A. .
TRENDS IN MOLECULAR MEDICINE, 2017, 23 (05) :411-429