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      Long Non-coding RNAs: Major Regulators of Cell Stress in Cancer


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          Cellular stress can occur in many forms; oxidative stress caused by reactive oxygen species (ROS), metabolic stress from increased metabolic programs and genotoxic stress in the form of DNA damage and disrepair. In most instances, these different types of cell stress initiate programmed cell death. However, in cancer, cells are able to resist cellular stress and by-pass growth limiting checkpoints. Recent findings have now revealed that the large and heterogenous RNA species known as long non-coding RNAs (lncRNAs) are major players in regulating and overcoming cancer cell stress. lncRNAs constitute a significant fraction of the genes differentially expressed in response to cell stress and contribute to the management of downstream cellular processes, including the regulation of key stress responses such as metabolic stress, oxidative stress and genotoxic stress. This review highlights the complex regulatory role of lncRNAs in the cell stress response of cancer by providing an overview of key examples from recent literature.

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          Most cited references24

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          Long noncoding RNA as modular scaffold of histone modification complexes.

          Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here, we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5' domain of HOTAIR binds polycomb repressive complex 2 (PRC2), whereas a 3' domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1 and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes.
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            NRF2 and the Hallmarks of Cancer

            The transcription factor NRF2 is the master regulator of the cellular antioxidant response. Though recognized originally as a target of chemopreventive compounds that help prevent cancer and other maladies, accumulating evidence has established the NRF2 pathway as a driver of cancer progression, metastasis, and resistance to therapy. Recent studies have identified new functions for NRF2 in the regulation of metabolism and other essential cellular functions, establishing NRF2 as a truly pleiotropic transcription factor. In this review, we explore the roles of NRF2 in the hallmarks of cancer, indicating both tumor suppressive and tumor-promoting effects.
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              The multiple mechanisms that regulate p53 activity and cell fate

              The tumour suppressor p53 has a central role in the response to cellular stress. Activated p53 transcriptionally regulates hundreds of genes that are involved in multiple biological processes, including in DNA damage repair, cell cycle arrest, apoptosis and senescence. In the context of DNA damage, p53 is thought to be a decision-making transcription factor that selectively activates genes as part of specific gene expression programmes to determine cellular outcomes. In this Review, we discuss the multiple molecular mechanisms of p53 regulation and how they modulate the induction of apoptosis or cell cycle arrest following DNA damage. Specifically, we discuss how the interaction of p53 with DNA and chromatin affects gene expression, and how p53 post-translational modifications, its temporal expression dynamics and its interactions with chromatin regulators and transcription factors influence cell fate. These multiple layers of regulation enable p53 to execute cellular responses that are appropriate for specific cellular states and environmental conditions.

                Author and article information

                Front Oncol
                Front Oncol
                Front. Oncol.
                Frontiers in Oncology
                Frontiers Media S.A.
                20 March 2020
                : 10
                : 285
                Children's Cancer Institute, School of Women's and Children's Health, Lowy Cancer Centre, University of New South Wales (UNSW) , Sydney, NSW, Australia
                Author notes

                Edited by: Sergio Giannattasio, Istituto di Biomembrane, Bioenergetica e Biotecnologie Molecolari (IBIOM), Italy

                Reviewed by: Graziano Pesole, University of Bari Aldo Moro, Italy; Claudia Cava, National Research Council, Italy

                *Correspondence: Patrick Connerty PConnerty@ 123456ccia.org.au
                Charles E. de Bock Cdebock@ 123456ccia.org.au

                This article was submitted to Molecular and Cellular Oncology, a section of the journal Frontiers in Oncology

                Copyright © 2020 Connerty, Lock and de Bock.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 02 December 2019
                : 18 February 2020
                Page count
                Figures: 2, Tables: 1, Equations: 0, References: 48, Pages: 7, Words: 5678
                Mini Review

                Oncology & Radiotherapy
                lncrna,metabolism,cell stress,oxidative stress,cancer,tumor suppressor gene,genotoxic stress


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