Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay

Arsenic is a global health concern at present and it is well reported for causing systemic toxicity. It is also well known for generation of free radical and inducing apoptosis in different cell types. Paradoxically arsenic is reported to be a susceptible carcinogen as well. There are several report...

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Main Authors:	Roy, Sonali, Narzary, Bardwi, Ray, Atish, Bordoloi, Manobjyoti
Format:	Online
Language:	English
Published:	Nature Publishing Group 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066266/

id	pubmed-5066266
recordtype	oai_dc
spelling	pubmed-50662662016-10-26 Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay Roy, Sonali Narzary, Bardwi Ray, Atish Bordoloi, Manobjyoti Article Arsenic is a global health concern at present and it is well reported for causing systemic toxicity. It is also well known for generation of free radical and inducing apoptosis in different cell types. Paradoxically arsenic is reported to be a susceptible carcinogen as well. There are several reports demonstrating diverse mechanism of apoptosis in different cell types. However, the universal scenario of instrumental genes and their interaction leading to amplification of apoptotic signal are yet to be completely uncovered, which is predicted here. Conventional studies on signaling pathway aided by time and concentration kinetics data are inadequate for prediction of anchored genes for apoptotic signal amplification. Therefore, expression profile-based approach is adopted. Core apoptosis related and glutathione metabolism genes in 1 and 10 μM of arsenic-treated HepG2 cells were analyzed after 12 h of incubation. An arsenic treatment of 1 μM exhibits no cell death at 12 h, whereas 10 μM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 μM arsenic-treated cells, respectively. Early initiation of apoptotic signaling is detected in no cell death regimens (at 1 μM), whereas amplified apoptotic signal is demonstrated at 50% cell death regimens (at 10 μM). Instrumental genes involved in progression of apoptosis in the concourse of cell death and survival is designated from the responsive genes common to both the condition. We predict the initiation process is fairly aided by the activation of intrinsic pathway, which is amplified via TNF signaling and extrinsic pathway. Furthermore, regulatory genes involved in interplay between apoptosis/anti-apoptosis and their interactions are demonstrated here. Nature Publishing Group 2016-10-17 /pmc/articles/PMC5066266/ /pubmed/27785370 http://dx.doi.org/10.1038/cddiscovery.2016.78 Text en Copyright © 2016 The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Roy, Sonali Narzary, Bardwi Ray, Atish Bordoloi, Manobjyoti
spellingShingle	Roy, Sonali Narzary, Bardwi Ray, Atish Bordoloi, Manobjyoti Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
author_facet	Roy, Sonali Narzary, Bardwi Ray, Atish Bordoloi, Manobjyoti
author_sort	Roy, Sonali
title	Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
title_short	Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
title_full	Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
title_fullStr	Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
title_full_unstemmed	Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
title_sort	arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay
description	Arsenic is a global health concern at present and it is well reported for causing systemic toxicity. It is also well known for generation of free radical and inducing apoptosis in different cell types. Paradoxically arsenic is reported to be a susceptible carcinogen as well. There are several reports demonstrating diverse mechanism of apoptosis in different cell types. However, the universal scenario of instrumental genes and their interaction leading to amplification of apoptotic signal are yet to be completely uncovered, which is predicted here. Conventional studies on signaling pathway aided by time and concentration kinetics data are inadequate for prediction of anchored genes for apoptotic signal amplification. Therefore, expression profile-based approach is adopted. Core apoptosis related and glutathione metabolism genes in 1 and 10 μM of arsenic-treated HepG2 cells were analyzed after 12 h of incubation. An arsenic treatment of 1 μM exhibits no cell death at 12 h, whereas 10 μM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 μM arsenic-treated cells, respectively. Early initiation of apoptotic signaling is detected in no cell death regimens (at 1 μM), whereas amplified apoptotic signal is demonstrated at 50% cell death regimens (at 10 μM). Instrumental genes involved in progression of apoptosis in the concourse of cell death and survival is designated from the responsive genes common to both the condition. We predict the initiation process is fairly aided by the activation of intrinsic pathway, which is amplified via TNF signaling and extrinsic pathway. Furthermore, regulatory genes involved in interplay between apoptosis/anti-apoptosis and their interactions are demonstrated here.
publisher	Nature Publishing Group
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066266/
_version_	1613686114601664512

Arsenic-induced instrumental genes of apoptotic signal amplification in death-survival interplay

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