2019
DOI: 10.1007/s40495-019-00171-y
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Role of Reactive Oxygen Species in Cancer Progression

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Cited by 56 publications
(22 citation statements)
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“…The obtained epidemiological and experimental data from the numerous studies supported Virchow’s hypothesis and revealed that inflammatory processes regulate the course of cancer based on the level of inflammation-related factors, inflammatory cytokines, and chemokines, in the tumor microenvironment, either by producing an antitumor response or by inducing cell transformation and malignancy [30,31,32]. One of the major regulatory components in the relationship between cancer and chronic inflammation is ROS that has an ability to affect the type, presence, and levels of inflammation-modulating factors such as activator protein 1 (AP-1), β-catenin/Wnt (wingless related integration site), HIF-1α (hypoxia-inducible factor-1 alpha), NF-κB, PPAR-γ (peroxisome proliferator-activated receptor gamma), p53, inflammatory cytokines, chemokines, and growth factors [27,33,34,35]. However, it should be noted that there is a complex crosstalk between chronic inflammation, ROS accumulation, and cancer progression (Figure 2).…”
Section: Role Of Ros In Cancer Progressionmentioning
confidence: 99%
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“…The obtained epidemiological and experimental data from the numerous studies supported Virchow’s hypothesis and revealed that inflammatory processes regulate the course of cancer based on the level of inflammation-related factors, inflammatory cytokines, and chemokines, in the tumor microenvironment, either by producing an antitumor response or by inducing cell transformation and malignancy [30,31,32]. One of the major regulatory components in the relationship between cancer and chronic inflammation is ROS that has an ability to affect the type, presence, and levels of inflammation-modulating factors such as activator protein 1 (AP-1), β-catenin/Wnt (wingless related integration site), HIF-1α (hypoxia-inducible factor-1 alpha), NF-κB, PPAR-γ (peroxisome proliferator-activated receptor gamma), p53, inflammatory cytokines, chemokines, and growth factors [27,33,34,35]. However, it should be noted that there is a complex crosstalk between chronic inflammation, ROS accumulation, and cancer progression (Figure 2).…”
Section: Role Of Ros In Cancer Progressionmentioning
confidence: 99%
“…This causes an increased mutation load, defects in signal-transduction, inactivation of apoptosis, and overpowered generation of additional ROS that activate the inflammation-modulating factors, inflammatory cytokines, and chemokines [34,35,36,37]. Apart from the induction of chronic inflammation by ROS-mediated NF-κB activation, the active NF-κB is considered to be a key component in the rise of therapy-resistant cancers toward fractional gamma-irradiation therapy and chemotherapeutic agents such as 5-fluorouracil, bortezomib, cisplatin, daunorubicin, doxorubicin, paclitaxel, vinblastine, vincristine, and tamoxifen, through the transcriptional up-regulation of Akt, Bcl-2 (B-cell lymphoma 2), Bcl-xL (B-cell lymphoma- extra-large), cyclin D1, COX-2, survivin, and XIAP (X-linked inhibitor of apoptosis) [38,39,40,41,42,43].…”
Section: Role Of Ros In Cancer Progressionmentioning
confidence: 99%
“…The level of intracellular ROS plays a crucial role in senescence occurrence (Panieri and Santoro, 2016), also closely associated with the principle of the metabolic process (Davalli et al, 2016) and various implications of cellular stress resulting from physiological maintenance of ROS metabolic enzymes in cancer cells (Kashyap et al, 2019). Several studies reported that out-level ROS over the threshold causes cell death or another type of permanent cell arrest as senescence (Ikawati et al, 2020;Larasati et al, 2018).…”
Section: Intracellular Ros Levelmentioning
confidence: 99%
“…Considerable changes in ROS levels can potentially disrupt cellular functions and effects are reversed by the actions of respiratory enzymes, that assist in quenching ROS [84] .Oxidative stress results from an overproduction of ROS with relatively low amounts of the antioxidant to defend the body from harmful effects of ROS [85] . It has been known that increased levels of ROS are dangerous as they tend to cause dysregulation of many cellular components involved in pathogenesis of several diseases [86][87][88][89] . Under such pathological states, synthetic or nature-based antioxidants are taken with the intent to reduce high levels of ROS.…”
Section: Assessment Of the Total Phenolic Contentmentioning
confidence: 99%