Oxidative stress-modulating drugs have preferential anticancer effects - involving the regulation of apoptosis, DNA damage, endoplasmic reticulum stress, autophagy, metabolism, and migration

To achieve preferential effects against cancer cells but less damage to normal cells is one of the main challenges of cancer research. In this review, we explore the roles and relationships of oxidative stress-mediated apoptosis, DNA damage, ER stress, autophagy, metabolism, and migration of ROS-mod...

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Published inSeminars in cancer biology Vol. 58; pp. 109 - 117
Main Authors Tang, Jen-Yang, Ou-Yang, Fu, Hou, Ming-Feng, Huang, Hurng-Wern, Wang, Hui-Ru, Li, Kun-Tzu, Fayyaz, Sundas, Shu, Chih-Wen, Chang, Hsueh-Wei
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.10.2019
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Online AccessGet full text
ISSN1044-579X
1096-3650
1096-3650
DOI10.1016/j.semcancer.2018.08.010

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Abstract To achieve preferential effects against cancer cells but less damage to normal cells is one of the main challenges of cancer research. In this review, we explore the roles and relationships of oxidative stress-mediated apoptosis, DNA damage, ER stress, autophagy, metabolism, and migration of ROS-modulating anticancer drugs. Understanding preferential anticancer effects in more detail will improve chemotherapeutic approaches that are based on ROS-modulating drugs in cancer treatments.
AbstractList To achieve preferential effects against cancer cells but less damage to normal cells is one of the main challenges of cancer research. In this review, we explore the roles and relationships of oxidative stress-mediated apoptosis, DNA damage, ER stress, autophagy, metabolism, and migration of ROS-modulating anticancer drugs. Understanding preferential anticancer effects in more detail will improve chemotherapeutic approaches that are based on ROS-modulating drugs in cancer treatments.To achieve preferential effects against cancer cells but less damage to normal cells is one of the main challenges of cancer research. In this review, we explore the roles and relationships of oxidative stress-mediated apoptosis, DNA damage, ER stress, autophagy, metabolism, and migration of ROS-modulating anticancer drugs. Understanding preferential anticancer effects in more detail will improve chemotherapeutic approaches that are based on ROS-modulating drugs in cancer treatments.
To achieve preferential effects against cancer cells but less damage to normal cells is one of the main challenges of cancer research. In this review, we explore the roles and relationships of oxidative stress-mediated apoptosis, DNA damage, ER stress, autophagy, metabolism, and migration of ROS-modulating anticancer drugs. Understanding preferential anticancer effects in more detail will improve chemotherapeutic approaches that are based on ROS-modulating drugs in cancer treatments.
Author Tang, Jen-Yang
Hou, Ming-Feng
Huang, Hurng-Wern
Shu, Chih-Wen
Chang, Hsueh-Wei
Wang, Hui-Ru
Ou-Yang, Fu
Li, Kun-Tzu
Fayyaz, Sundas
Author_xml – sequence: 1
  givenname: Jen-Yang
  surname: Tang
  fullname: Tang, Jen-Yang
  email: reyata@kmu.edu.tw
  organization: Department of Radiation Oncology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
– sequence: 2
  givenname: Fu
  surname: Ou-Yang
  fullname: Ou-Yang, Fu
  email: swfuon@kmu.edu.tw
  organization: Division of Breast Surgery and Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
– sequence: 3
  givenname: Ming-Feng
  surname: Hou
  fullname: Hou, Ming-Feng
  email: mifeho@kmu.edu.tw
  organization: Division of Breast Surgery and Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
– sequence: 4
  givenname: Hurng-Wern
  surname: Huang
  fullname: Huang, Hurng-Wern
  email: sting@mail.nsysu.edu.tw
  organization: Institute of Biomedical Science, National Sun Yat-sen University, Kaohsiung, Taiwan
– sequence: 5
  givenname: Hui-Ru
  surname: Wang
  fullname: Wang, Hui-Ru
  email: hr_wang@g-mail.nsysu.edu.tw
  organization: Institute of Biomedical Science, National Sun Yat-sen University, Kaohsiung, Taiwan
– sequence: 6
  givenname: Kun-Tzu
  surname: Li
  fullname: Li, Kun-Tzu
  email: ed109552@edah.org.tw
  organization: Department of Biomedical Science and Environmental Biology, Kaohsiung Medical University, Kaohsiung, Taiwan
– sequence: 7
  givenname: Sundas
  surname: Fayyaz
  fullname: Fayyaz, Sundas
  email: sundas.khan23@yahoo.com
  organization: Laboratory for Translational Oncology and Personalized Medicine, Rashid Latif Medical College (RLMC), Lahore, Pakistan
– sequence: 8
  givenname: Chih-Wen
  surname: Shu
  fullname: Shu, Chih-Wen
  email: cwshu@isu.edu.tw
  organization: School of Medicine for International Students, I-Shou University, Kaohsiung, Taiwan
– sequence: 9
  givenname: Hsueh-Wei
  orcidid: 0000-0003-0068-2366
  surname: Chang
  fullname: Chang, Hsueh-Wei
  email: changhw@kmu.edu.tw
  organization: Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30149066$$D View this record in MEDLINE/PubMed
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IsScholarly true
Keywords Anticancer drugs
Oxidative stress
Function
Preferential killing
Redox homeostasis
Language English
License Copyright © 2018 Elsevier Ltd. All rights reserved.
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PublicationTitle Seminars in cancer biology
PublicationTitleAlternate Semin Cancer Biol
PublicationYear 2019
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Snippet To achieve preferential effects against cancer cells but less damage to normal cells is one of the main challenges of cancer research. In this review, we...
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SubjectTerms Animals
Anticancer drugs
Antineoplastic Agents - pharmacology
Antineoplastic Agents - therapeutic use
Autophagy - drug effects
Cell Movement - drug effects
DNA Damage - drug effects
Endoplasmic Reticulum Stress - drug effects
Function
Humans
Oxidative stress
Oxidative Stress - drug effects
Preferential killing
Redox homeostasis
Title Oxidative stress-modulating drugs have preferential anticancer effects - involving the regulation of apoptosis, DNA damage, endoplasmic reticulum stress, autophagy, metabolism, and migration
URI https://www.clinicalkey.com/#!/content/1-s2.0-S1044579X18300841
https://dx.doi.org/10.1016/j.semcancer.2018.08.010
https://www.ncbi.nlm.nih.gov/pubmed/30149066
https://www.proquest.com/docview/2095538394
Volume 58
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