2018
DOI: 10.1016/j.canlet.2017.11.002
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Oxidative stress and dietary phytochemicals: Role in cancer chemoprevention and treatment

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Cited by 454 publications
(314 citation statements)
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“…Importantly, many phytochemicals have been shown to suppress cellular signaling pathways and promote cancer cell death. They behave like pro-oxidants, increasing oxidative stress in cancer cells by inhibiting ROS scavenging system, inactivating pro-survival signaling pathways, and finally triggering apoptotic cell death [7]. Bioflavonoids are a large group of bioactive compounds that mediate antitumor effects in many cancer models.…”
Section: Introductionmentioning
confidence: 99%
“…Importantly, many phytochemicals have been shown to suppress cellular signaling pathways and promote cancer cell death. They behave like pro-oxidants, increasing oxidative stress in cancer cells by inhibiting ROS scavenging system, inactivating pro-survival signaling pathways, and finally triggering apoptotic cell death [7]. Bioflavonoids are a large group of bioactive compounds that mediate antitumor effects in many cancer models.…”
Section: Introductionmentioning
confidence: 99%
“…Moreover, ROS activates several molecules and affects multiple cellular processes such as apoptosis, proliferation and gene expression . Oxidative stress can trigger carcinogenesis and damage cells and is significant in tumor expansion . Several toxic agents including inflammatory cytokines, irradiation and chemical oncogens induce ROS formation and thereby change redox potential, and can activate various signaling pathways.…”
Section: The Mechanisms Of Leukemia Pathogenesismentioning
confidence: 99%
“…During the promotion stage, oxidation of methionine and cysteine residues in proteins can affect their structure and enzymatic activities that result in deregulation of some signaling pathways, such as RAS‐MEK‐ERK1/2, phosphoinositide 3‐kinase (PI3K)/AKT, Keap1‐Nrf2‐ARE, nuclear factor ÎșB, and JAK/STAT . Toward inactivation of phosphatases by ROS‐mediated oxidation of the reactive cysteine thiol at their catalytic site, they are unable to dephosphorylate, and cannot inactivate target proteins, such as those belonging to RAS‐MEK‐ERK and PI3K/AKT signaling pathways . Thus, elevated levels of ROS by generating genomic instability, contribute to the progression phase of carcinogenesis.…”
Section: Mechanisms Of Os In Cancer: Trace Elements Implicationmentioning
confidence: 99%
“…To limit these toxic effects of ROS in response to OS, various oncogenes also increase the expression of nuclear factor E2‐related factor 2 (Nrf2), which stimulates tumorigenesis and reduces ROS levels . Intracellular ROS reduction is regulated by antioxidant enzymes such as SODs, catalase (CAT), heme oxygenase‐1 (HMOX‐1), glutathione peroxidase (GPx), thioredoxins (TXN), thioredoxin reductase (TRXR), peroxiredoxins (PRDx), NAD(P)H quinone oxidoreductase 1 (NQO1), and glutathione‐ S ‐transferase (GSTs) . The content and activity of enzymatic antioxidants are associated with the concentration of trace elements .…”
Section: Mechanisms Of Os In Cancer: Trace Elements Implicationmentioning
confidence: 99%