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Title:
Induction of reactive oxygen species: an emerging approach for cancer therapy | Apoptosis
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Reactive oxygen species (ROS), a group of ions and molecules, include hydroxyl radicals (Β·OH), alkoxyl radicals, superoxide anion (O2Β·β), singlet oxygen (1O2) and hydrogen peroxide (H2O2). Hydroxyl radicals and alkoxyl radicals are extremely and highly reactive species respectively. Endogenous ROS are mainly formed in mitochondrial respiratory chain. Low levels of ROS play important roles in regulating biological functions in mammalian cells. However, excess production of ROS can induce cell death by oxidative damaging effects to intracellular biomacromolecules. Cancer cell death types induced by ROS include apoptotic, autophagic, ferroptotic and necrotic cell death. Since abnormal metabolism in cancer cells, they have higher ROS content compared to normal cells. The higher endogenous ROS levels in cancer cells endow them more susceptible to the ROS-induction treatment. Indeed, some anticancer drugs currently used in clinic, such as molecular targeted drugs and chemotherapeutic agents, effectively kill cancer cells by inducing ROS generation. In addition, photodynamic therapy (PDT) is mainly based on induction of ROS burst to kill cancer cells. The mechanism of cell death induced by radiotherapy using ionizing radiation also refers to ROS production. Moreover, ROS play an important role in tumor immune therapy. Altogether, combining above traditional treatments with ROS-induced agents will be considered as a promising strategy in cancer therapy. In this review, we focus on our current understanding of the anticancer effects of ROS.
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pubmed, google, scholar, article, cas, cancer, cell, cells, central, apoptosis, ros, reactive, oxygen, biol, wang, death, species, therapy, zhang, mitochondrial, pathway, med, oxidative, stress, signaling, autophagy, zou, chen, induces, activation, redox, human, mol, res, yang, free, expression, induction, induced, immunol, production, nat, radic, synergistic, resistance, chem, liu, breast, lung, anticancer,
Topics {βοΈ}
p-eif2alpha/atf4/chop axis month download article/chapter c-myc-nrf2-keap1 pathway proteasome inhibitor-induced cleavage reactive oxygen species-dependent blocking nf-kappab sensitizes myeloid-derived suppressor cells intestinal p-glycoprotein expression nox-family nadph oxidases ros-mediated mitochondrial pathway nf-kappab/fasl pathway histone deacetylase inhibitor ca2+-coupled mitochondrial processes photofrin-mediated photodynamic therapy p53-ros cross-talk jnk/p38 map kinases her2-positive breast cancer sun yat-sen university fludarabine-resistant cll cells cell receptor-signaling pathways ros-mediated cellular signaling artesunate-induced ferroptosis cell death induced reactive oxygen species c6 glioma cells proline oxidase activates full article pdf endoplasmic reticulum stress induce cell death article apoptosis aims programmed death-1 controls electron transport complex p-glycoprotein expression resveratrol synergistically enhances vdac-dependent permeabilization fas ligand expression highly reactive species ph-triggered chemotherapy metabolic inhibitors accentuate necrotic cell death nonapoptotic cell death immunogenic cell death therapy-resistant state mitochondrial membrane permeabilization mitochondrial calcium handling superoxide induces rapid fas ligand promoter mitochondrial ros production mediated oxidative stress pci-24781 induces caspase
Questions {β}
- Trachootham D, Alexandre J, Huang P (2009) Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?
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headline:Induction of reactive oxygen species: an emerging approach for cancer therapy
description:Reactive oxygen species (ROS), a group of ions and molecules, include hydroxyl radicals (Β·OH), alkoxyl radicals, superoxide anion (O2Β·β), singlet oxygen (1O2) and hydrogen peroxide (H2O2). Hydroxyl radicals and alkoxyl radicals are extremely and highly reactive species respectively. Endogenous ROS are mainly formed in mitochondrial respiratory chain. Low levels of ROS play important roles in regulating biological functions in mammalian cells. However, excess production of ROS can induce cell death by oxidative damaging effects to intracellular biomacromolecules. Cancer cell death types induced by ROS include apoptotic, autophagic, ferroptotic and necrotic cell death. Since abnormal metabolism in cancer cells, they have higher ROS content compared to normal cells. The higher endogenous ROS levels in cancer cells endow them more susceptible to the ROS-induction treatment. Indeed, some anticancer drugs currently used in clinic, such as molecular targeted drugs and chemotherapeutic agents, effectively kill cancer cells by inducing ROS generation. In addition, photodynamic therapy (PDT) is mainly based on induction of ROS burst to kill cancer cells. The mechanism of cell death induced by radiotherapy using ionizing radiation also refers to ROS production. Moreover, ROS play an important role in tumor immune therapy. Altogether, combining above traditional treatments with ROS-induced agents will be considered as a promising strategy in cancer therapy. In this review, we focus on our current understanding of the anticancer effects of ROS.
datePublished:2017-09-21T00:00:00Z
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description:Reactive oxygen species (ROS), a group of ions and molecules, include hydroxyl radicals (Β·OH), alkoxyl radicals, superoxide anion (O2Β·β), singlet oxygen (1O2) and hydrogen peroxide (H2O2). Hydroxyl radicals and alkoxyl radicals are extremely and highly reactive species respectively. Endogenous ROS are mainly formed in mitochondrial respiratory chain. Low levels of ROS play important roles in regulating biological functions in mammalian cells. However, excess production of ROS can induce cell death by oxidative damaging effects to intracellular biomacromolecules. Cancer cell death types induced by ROS include apoptotic, autophagic, ferroptotic and necrotic cell death. Since abnormal metabolism in cancer cells, they have higher ROS content compared to normal cells. The higher endogenous ROS levels in cancer cells endow them more susceptible to the ROS-induction treatment. Indeed, some anticancer drugs currently used in clinic, such as molecular targeted drugs and chemotherapeutic agents, effectively kill cancer cells by inducing ROS generation. In addition, photodynamic therapy (PDT) is mainly based on induction of ROS burst to kill cancer cells. The mechanism of cell death induced by radiotherapy using ionizing radiation also refers to ROS production. Moreover, ROS play an important role in tumor immune therapy. Altogether, combining above traditional treatments with ROS-induced agents will be considered as a promising strategy in cancer therapy. In this review, we focus on our current understanding of the anticancer effects of ROS.
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