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Author Xiang, S.; Dauchy, R.T.; Hoffman, A.E.; Pointer, D.; Frasch, T.; Blask, D.E.; Hill, S.M.
Title Epigenetic inhibition of the tumor suppressor ARHI by light at night-induced circadian melatonin disruption mediates STAT3-driven paclitaxel resistance in breast cancer Type Journal Article
Year 2019 Publication Journal of Pineal Research Abbreviated Journal J Pineal Res
Volume 67 Issue 2 Pages e12586
Keywords (up) Animals; Human Health; Circadian Rhythm; Cancer; tumor suppression
Abstract Disruption of circadian time structure and suppression of circadian nocturnal melatonin (MLT) production by exposure to dim light at night (dLAN), as occurs with night shift work and/or disturbed sleep-wake cycles, is associated with a significantly increased risk of breast cancer and resistance to tamoxifen and doxorubicin. Melatonin inhibition of human breast cancer chemo-resistance involves mechanisms including suppression of tumor metabolism and inhibition of kinases and transcription factors which are often activated in drug-resistant breast cancer. Signal Transducer and Activator of Transcription 3 (STAT3), frequently overexpressed and activated in Paclitaxel (PTX)-resistant breast cancer, promotes the expression of DNA methyltransferase one (DNMT1) to epigenetically suppresses the transcription of tumor suppressor Aplasia Ras homolog one (ARHI) which can sequester STAT3 in the cytoplasm to block PTX-resistance. We demonstrate that breast tumor xenografts in rats exposed to dLAN and circadian MLT disrupted express elevated levels of phosphorylated and acetylated STAT3, increased DNMT1, but reduced Sirtuin 1 (SIRT1) and ARHI. Furthermore, MLT and/or SIRT1 administration blocked/reversed Interleukin 6 (IL-6)-induced acetylation of STAT3 and its methylation of ARH1 to increase ARH1 mRNA expression in MCF-7 breast cancer cells. Finally, analyses of the I-SPY 1 trial demonstrates that elevated MT1 receptor expression is significantly correlated with pathologic complete response following neo-adjuvant therapy in breast cancer patients. This is the first study to demonstrate circadian disruption of MLT by dLAN driving intrinsic resistance to PTX via epigenetic mechanisms increasing STAT3 expression and that MLT administration can reestablish sensitivity of breast tumors to PTX and drive tumor regression.
Address Tulane Circadian Cancer Biology Group, New Orleans, Louisiana
Corporate Author Thesis
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Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0742-3098 ISBN Medium
Area Expedition Conference
Notes PMID:31077613 Approved no
Call Number GFZ @ kyba @ Serial 2383
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Author Nicholls, S. K., Casiraghi, L. P., Wang. W., Weber, E. T., & Harrington, M. E.
Title Evidence for Internal Desynchrony Caused by Circadian Clock Resetting Type Journal Article
Year 2019 Publication Yale Journal of Biology and Medicine Abbreviated Journal
Volume 92 Issue 2 Pages 259-270
Keywords (up) Animals; Human Health; Review
Abstract Circadian disruption has been linked to markers for poor health outcomes in humans and animal models. What is it about circadian disruption that is problematic? One hypothesis is that phase resetting of the circadian system, which occurs in response to changes in environmental timing cues, leads to internal desynchrony within the organism. Internal desynchrony is understood as acute changes in phase relationships between biological rhythms from different cell groups, tissues, or organs within the body. Do we have strong evidence for internal desynchrony associated with or caused by circadian clock resetting? Here we review the literature, highlighting several key studies from measures of gene expression in laboratory rodents. We conclude that current evidence offers strong support for the premise that some protocols for light-induced resetting are associated with internal desynchrony. It is important to continue research to test whether internal desynchrony is necessary and/or sufficient for negative health impact of circadian disruption.
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Language Summary Language Original Title
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ISSN ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ intern @ Serial 2631
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Author Khan, Z.A.; Yumnamcha, T.; Mondal, G.; Devi, S.D.; Rajiv, C.; Labala, R.K.; Sanjita Devi, H.; Chattoraj, A.
Title Artificial Light at Night (ALAN): A Potential Anthropogenic Component for the COVID-19 and HCoVs Outbreak Type Journal Article
Year 2020 Publication Frontiers in Endocrinology Abbreviated Journal Front Endocrinol (Lausanne)
Volume 11 Issue Pages 622
Keywords (up) Animals; Human Health; Review; ALAN; Covid-19; HCoVs; bat; melatonin; sustainability
Abstract The origin of the coronavirus disease 2019 (COVID-19) pandemic is zoonotic. The circadian day-night is the rhythmic clue to organisms for their synchronized body functions. The “development for mankind” escalated the use of artificial light at night (ALAN). In this article, we tried to focus on the possible influence of this anthropogenic factor in human coronavirus (HCoV) outbreak. The relationship between the occurrences of coronavirus and the ascending curve of the night-light has also been delivered. The ALAN influences the physiology and behavior of bat, a known nocturnal natural reservoir of many Coronaviridae. The “threatened” and “endangered” status of the majority of bat species is mainly because of the destruction of their proper habit and habitat predominantly through artificial illumination. The stress exerted by ALAN leads to the impaired body functions, especially endocrine, immune, genomic integration, and overall rhythm features of different physiological variables and behaviors in nocturnal animals. Night-light disturbs “virus-host” synchronization and may lead to mutation in the genomic part of the virus and excessive virus shedding. We also proposed some future strategies to mitigate the repercussions of ALAN and for the protection of the living system in the earth as well.
Address Biological Rhythm Laboratory, Department of Animal Science, Kazi Nazrul University, Asansol, India
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1664-2392 ISBN Medium
Area Expedition Conference
Notes PMID:33013700; PMCID:PMC7511708 Approved no
Call Number GFZ @ kyba @ Serial 3169
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Author Walker, W.H. 2nd; Borniger, J.C.; Gaudier-Diaz, M.M.; Hecmarie Melendez-Fernandez, O.; Pascoe, J.L.; Courtney DeVries, A.; Nelson, R.J.
Title Acute exposure to low-level light at night is sufficient to induce neurological changes and depressive-like behavior Type Journal Article
Year 2019 Publication Molecular Psychiatry Abbreviated Journal Mol Psychiatry
Volume Issue Pages s41380
Keywords (up) Animals; mouse models; mood disorders; Human Health
Abstract The advent and wide-spread adoption of electric lighting over the past century has profoundly affected the circadian organization of physiology and behavior for many individuals in industrialized nations; electric lighting in homes, work environments, and public areas have extended daytime activities into the evening, thus, increasing night-time exposure to light. Although initially assumed to be innocuous, chronic exposure to light at night (LAN) is now associated with increased incidence of cancer, metabolic disorders, and affective problems in humans. However, little is known about potential acute effects of LAN. To determine whether acute exposure to low-level LAN alters brain function, adult male, and female mice were housed in either light days and dark nights (LD; 14 h of 150 lux:10 h of 0 lux) or light days and low level light at night (LAN; 14 h of 150 lux:10 h of 5 lux). Mice exposed to LAN on three consecutive nights increased depressive-like responses compared to mice housed in dark nights. In addition, female mice exposed to LAN increased central tendency in the open field. LAN was associated with reduced hippocampal vascular endothelial growth factor-A (VEGF-A) in both male and female mice, as well as increased VEGFR1 and interleukin-1beta mRNA expression in females, and reduced brain derived neurotrophic factor mRNA in males. Further, LAN significantly altered circadian rhythms (activity and temperature) and circadian gene expression in female and male mice, respectively. Altogether, this study demonstrates that acute exposure to LAN alters brain physiology and can be detrimental to well-being in otherwise healthy individuals.
Address Department of Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, 26506, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1359-4184 ISBN Medium
Area Expedition Conference
Notes PMID:31138889; PMCID:PMC6881534 Approved no
Call Number GFZ @ kyba @ Serial 2768
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Author Walker, W.H. 2nd; Melendez-Fernandez, O.H.; Nelson, R.J.
Title Prior exposure to dim light at night impairs dermal wound healing in female C57BL/6 mice Type Journal Article
Year 2019 Publication Archives of Dermatological Research Abbreviated Journal Arch Dermatol Res
Volume 311 Issue 7 Pages 573-576
Keywords (up) Animals; mouse models; Skin; Human Health
Abstract Artificial light at night (LAN) is a pervasive phenomenon in today's society, and the detrimental consequences of LAN exposure are becoming apparent. LAN is associated with the increased incidence of metabolic disorders, cancers, mood alterations, and immune dysfunction in mammals. Consequently, we examined the effects of dim LAN (DLAN) on wound healing. Female C57BL/6 mice were housed for 3 weeks in DLAN or LD conditions prior to wounding. Following wounding, mice were maintained in either their previous light conditions or switched to the opposite lighting conditions for 3 weeks. DLAN prior to wounding impaired healing; specifically, mice in DLAN/DLAN had significantly larger wounds on day 8. Additionally, mice in DLAN/LD had significantly larger wounds on days 5, 7, 8, and 9, and increased average time to closure. These data demonstrate a potential harmful effect of DLAN on wound healing that should be considered and may represent a target for therapeutic intervention.
Address Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, 26506, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0340-3696 ISBN Medium
Area Expedition Conference
Notes PMID:31144020 Approved no
Call Number GFZ @ kyba @ Serial 2515
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