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

Authors: Lu, Wei-Cheng  Xie, Hui  Tie, Xin-Xin  Wang, Ruizhe  Wu, An-Hua  Shan, Feng-Ping 
Citation: Lu WC, etal., Int Immunopharmacol. 2018 Mar;56:1-8. doi: 10.1016/j.intimp.2018.01.005. Epub 2018 Jan 9.
Pubmed: (View Article at PubMed) PMID:29324390
DOI: Full-text: DOI:10.1016/j.intimp.2018.01.005

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.

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CRRD Object Information
CRRD ID: 13792598
Created: 2018-09-17
Species: All species
Last Modified: 2018-09-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.