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

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          Abstract

          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.

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          Most cited references174

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          Cell death: critical control points.

          Programmed cell death is a distinct genetic and biochemical pathway essential to metazoans. An intact death pathway is required for successful embryonic development and the maintenance of normal tissue homeostasis. Apoptosis has proven to be tightly interwoven with other essential cell pathways. The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics.
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            Role of reactive oxygen species (ROS) in apoptosis induction.

            Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.
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              Targeting microRNAs in cancer: rationale, strategies and challenges.

              MicroRNAs (miRNAs) are evolutionarily conserved small non-coding RNAs that regulate gene expression. Early studies have shown that miRNA expression is deregulated in cancer and experimental data indicate that cancer phenotypes can be modified by targeting miRNA expression. Based on these observations, miRNA-based anticancer therapies are being developed, either alone or in combination with current targeted therapies, with the goal to improve disease response and increase cure rates. The advantage of using miRNA approaches is based on its ability to concurrently target multiple effectors of pathways involved in cell differentiation, proliferation and survival. In this Review, we describe the role of miRNAs in tumorigenesis and critically discuss the rationale, the strategies and the challenges for the therapeutic targeting of miRNAs in cancer.
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                Author and article information

                Journal
                Biomolecules
                Biomolecules
                biomolecules
                Biomolecules
                MDPI
                2218-273X
                13 November 2019
                November 2019
                : 9
                : 11
                : 735
                Affiliations
                [1 ]Department of Histopathology, Post Graduate Institute of Medical Education and Research (PGIMER), Punjab, Chandigarh 160012, India; vaishali.pgi@ 123456gmail.com
                [2 ]Department of Biotechnology, Maharishi Markandeshwar (Deemed to be University), Mullana, Ambala, Haryana 133207, India; thakralfalak@ 123456gmail.com
                [3 ]Department of Pharmacology, Faculty of Pharmacy, Anadolu University, Eskişehir TR26470, Turkey; aysegulv@ 123456anadolu.edu.tr
                [4 ]Department of Pharmacology, Faculty of Pharmacy, Erciyes University, Kayseri 38039, Turkey; eczbetul@ 123456yahoo.com
                [5 ]NGO Praeventio, Tartu 50407, Estonia; katrin.sak.001@ 123456mail.ee
                [6 ]Department of Molecular Biology and Genetics, Faculty of Science, Kotekli Campus, Mugla Sitki Kocman University, Mugla TR48000, Turkey; mehmetvarol@ 123456mu.edu.tr
                [7 ]Department of Animal Sciences, Central University of Punjab, City Campus, Mansa Road, Bathinda 151001, India; aklankjain@ 123456gmail.com
                [8 ]The Research Center for Preclinical Medicine, Southwest Medical University, Luzhou 646000, Sichuan, China; asadkhan@ 123456swmu.edu.cn
                [9 ]Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore
                Author notes
                [* ]Correspondence: hardeep.biotech@ 123456gmail.com (H.S.T.); phcgs@ 123456nus.edu.sg (G.S.); Tel.: +91-9896619923 (H.S.T.); +65-6516-3267 (G.S.)
                Author information
                https://orcid.org/0000-0002-4503-8032
                https://orcid.org/0000-0003-0736-2525
                https://orcid.org/0000-0003-2565-453X
                https://orcid.org/0000-0001-5539-3225
                https://orcid.org/0000-0001-7851-0500
                Article
                biomolecules-09-00735
                10.3390/biom9110735
                6920770
                31766246
                30a1d55c-73df-47a7-af1d-eb7ea15c2e08
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 24 October 2019
                : 12 November 2019
                Categories
                Review

                reactive oxygen species (ros),oxidative stress,inflammation,angiogenesis,metastasis,mirna

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