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. 2016 Dec 7;23:88. doi: 10.1186/s12929-016-0306-8

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — A schematic representation of the role of COX-2 (Cyclooxigenases-2) in proliferation of cancer cells. Radiation as well as PGE2 (Prostaglandin E2) are able to transactivate EGFR (Epidermal Growth Factor Receptor) that upregulates the level of pro- survival protein through PI3K/AKT, MAPK/ERK and JAK/STAT pathways. Also, caspase activation leads to release of arachidonic acid