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Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements

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Department of Histopathology, Post Graduate Institute of Medical Education and Research (PGIMER), Punjab, Chandigarh 160012, India
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Department of Biotechnology, Maharishi Markandeshwar (Deemed to be University), Mullana, Ambala, Haryana 133207, India
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Department of Pharmacology, Faculty of Pharmacy, Anadolu University, Eskişehir TR26470, Turkey
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Department of Pharmacology, Faculty of Pharmacy, Erciyes University, Kayseri 38039, Turkey
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NGO Praeventio, Tartu 50407, Estonia
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Department of Molecular Biology and Genetics, Faculty of Science, Kotekli Campus, Mugla Sitki Kocman University, Mugla TR48000, Turkey
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Department of Animal Sciences, Central University of Punjab, City Campus, Mansa Road, Bathinda 151001, India
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The Research Center for Preclinical Medicine, Southwest Medical University, Luzhou 646000, Sichuan, China
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Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore
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Authors to whom correspondence should be addressed.
Biomolecules 2019, 9(11), 735; https://doi.org/10.3390/biom9110735
Received: 24 October 2019 / Revised: 11 November 2019 / Accepted: 12 November 2019 / Published: 13 November 2019
(This article belongs to the Special Issue Antitumor Agents from Natural Sources)
Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies. View Full-Text
Keywords: reactive oxygen species (ROS); oxidative stress; inflammation; angiogenesis; metastasis; miRNA reactive oxygen species (ROS); oxidative stress; inflammation; angiogenesis; metastasis; miRNA
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Aggarwal, V.; Tuli, H.S.; Varol, A.; Thakral, F.; Yerer, M.B.; Sak, K.; Varol, M.; Jain, A.; Khan, M.A.; Sethi, G. Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements. Biomolecules 2019, 9, 735.

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