NFAT-1 hyper-activation by methionine enkephalin (MENK) significantly induces cell apoptosis of rats C6 glioma in vivo and in vitro

NFAT-1 hyper-activation by methionine enkephalin (MENK) significantly induces cell apoptosis of... The aim of the work was to investigate the effect and possible mechanism of MENK on the growth of rat C6 glioma in vivo or in vitro. Our findings showed that MENK could inhibit the growth of rat C6 glioma, prolong median survival times in tumor-bearing rats, and induce glioma cell apoptosis. Moreover, MENK could increase the activities of caspase-3, caspase-8 and caspase-9. It also increased the expression of Fas, FasL, Bax, while decreased the expression of Bcl-2. We further confirmed that MENK could increase opioid receptors MOR and DOR expressions, Ca2+ influx into the cytoplasm, and a substantial increase of NFAT1accumulation in the nuclei in C6 glioma cell. When we specifically knocked down NFAT1, there was no effect of MENK on the cell viability and FasL up-regulation in NFAT1 knocked-down cell. These results demonstrate that MENK could bind to opioid receptors MOR and DOR on C6 glioma cells and trigger a Ca2+ influx into the cytoplasm, resulting in translocation of NFAT1 into the nucleus. The hyper-activation of NFAT1 may regulate transcription of downstream gene, such as FasL, and induce apoptosis of rat C6 glioma cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Immunopharmacology Elsevier

NFAT-1 hyper-activation by methionine enkephalin (MENK) significantly induces cell apoptosis of rats C6 glioma in vivo and in vitro

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Publisher
Elsevier
Copyright
Copyright © 2018 Elsevier B.V.
ISSN
1567-5769
eISSN
1878-1705
D.O.I.
10.1016/j.intimp.2018.01.005
Publisher site
See Article on Publisher Site

Abstract

The aim of the work was to investigate the effect and possible mechanism of MENK on the growth of rat C6 glioma in vivo or in vitro. Our findings showed that MENK could inhibit the growth of rat C6 glioma, prolong median survival times in tumor-bearing rats, and induce glioma cell apoptosis. Moreover, MENK could increase the activities of caspase-3, caspase-8 and caspase-9. It also increased the expression of Fas, FasL, Bax, while decreased the expression of Bcl-2. We further confirmed that MENK could increase opioid receptors MOR and DOR expressions, Ca2+ influx into the cytoplasm, and a substantial increase of NFAT1accumulation in the nuclei in C6 glioma cell. When we specifically knocked down NFAT1, there was no effect of MENK on the cell viability and FasL up-regulation in NFAT1 knocked-down cell. These results demonstrate that MENK could bind to opioid receptors MOR and DOR on C6 glioma cells and trigger a Ca2+ influx into the cytoplasm, resulting in translocation of NFAT1 into the nucleus. The hyper-activation of NFAT1 may regulate transcription of downstream gene, such as FasL, and induce apoptosis of rat C6 glioma cells.

Journal

International ImmunopharmacologyElsevier

Published: Mar 1, 2018

References

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