TY - CHAP
T1 - The Regulation of Pathways of Inflammation and Resolution in Immune Cells and Cancer Stem Cells by Selenium
AU - Diwakar, Bastihalli T.
AU - Korwar, Arvind M.
AU - Paulson, Robert F.
AU - Prabhu, K. Sandeep
N1 - Funding Information:
This work was supported, in part, by grants from the National Institutes of Health R01CA162665, R01DK077152, Office of Dietary Supplements (ODS-NIH), USDA-NIFA Hatch project numbers 4605 (K.S.P.) and 4736 (R.F.P.). We thank current and former members of the Prabhu laboratory for their invaluable contributions.
Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017
Y1 - 2017
N2 - Cancer is a complex disease where cancer stem cells (CSCs) maintain unlimited replicative potential, but evade chemotherapy drugs through cellular quiescence. CSCs are able to give rise to bulk tumor cells that have the capability to override antiproliferative signals and evade apoptosis. Numerous pathways are dysregulated in tumor cells, where increased levels of prooxidant reactive oxygen and nitrogen species can lead to localized inflammation to exacerbate all three stages of tumorigenesis: initiation, progression, and metastasis. Modulation of cellular metabolism in tumor cells as well as immune cells in the tumor microenvironment (TME) can impact inflammatory networks. Altering these pathways can potentially serve as a portal for therapy. It is well known that selenium, through selenoproteins, modulates inflammatory pathways in addition to regulating redox homeostasis in cells. Therefore, selenium has the potential to impact the interaction between tumor cells, CSCs, and immune cells. In the sections later, we review the current status of knowledge regarding this interaction, with reference to leukemia stem cells, and the importance of selenium-dependent regulation of inflammation as a potential mechanism to affect the TME and tumor cell survival.
AB - Cancer is a complex disease where cancer stem cells (CSCs) maintain unlimited replicative potential, but evade chemotherapy drugs through cellular quiescence. CSCs are able to give rise to bulk tumor cells that have the capability to override antiproliferative signals and evade apoptosis. Numerous pathways are dysregulated in tumor cells, where increased levels of prooxidant reactive oxygen and nitrogen species can lead to localized inflammation to exacerbate all three stages of tumorigenesis: initiation, progression, and metastasis. Modulation of cellular metabolism in tumor cells as well as immune cells in the tumor microenvironment (TME) can impact inflammatory networks. Altering these pathways can potentially serve as a portal for therapy. It is well known that selenium, through selenoproteins, modulates inflammatory pathways in addition to regulating redox homeostasis in cells. Therefore, selenium has the potential to impact the interaction between tumor cells, CSCs, and immune cells. In the sections later, we review the current status of knowledge regarding this interaction, with reference to leukemia stem cells, and the importance of selenium-dependent regulation of inflammation as a potential mechanism to affect the TME and tumor cell survival.
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U2 - 10.1016/bs.acr.2017.07.003
DO - 10.1016/bs.acr.2017.07.003
M3 - Chapter
C2 - 29054417
AN - SCOPUS:85027977986
T3 - Advances in Cancer Research
SP - 153
EP - 172
BT - Advances in Cancer Research
PB - Academic Press Inc.
ER -