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M Tu
W Zheng

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M Tu
W Zheng

International Research Journal of Medicine and Biomedical Sciences
Vol.3 (1),pp. 1-4, May 2018
ISSN 2488-9032
Available online at https://www.journalissues.org/IRJMBS/
DOI:https://doi.org/10.15739/irjmbs.18.001
Author(s) retain the copyright of this article. Author(s) agree that this article remain permanently open access under the terms of the Creative Commons Attribution License 4.0 International License.



Original Research Article

CD164 induced the apoptosis of U87 cell by down-regulating PTEN/PI3K/AKT signal pathway in vitro

Ming Tu*1 and Weiming Zheng1

1The first hospital affiliated to Wenzhou Medical University, Wenzhou, China.

*Corresponding Author Email: wzfeytm(at)163.com



date Received: March 9, 2018     date Accepted: April 23, 2018     date Published: April 28, 2018


 Abstract

To investigate CD164 induced the apoptosis of U87 cell by down-regulating PTEN/PI3K/AKT signal pathway in vitro. Human CD164 sequence was used for the design of shRNA targeting CD164, which was then introduced to lentivirus, followed by transfection into U87 cells. The CCK-8 was used to investigate whether silencing of CD164 exert anti-proliferative and pro-apoptotic effects on U87 cells. Western blot assay was used to detect the expression of PTEN, p-AKT and p53 in U87 cells. After transfection with CD164 shRNA in U87 cells, human glioma cell line U87 with down-regulation of CD164 showed significant inhibition of cell proliferation compared with shRNA NC (P<0.001). Furthermore, CCK 8 result showed that apoptosis rate induced by the CD164 shRNA transfection was markedly higher than that of control (P<0.001). The western blot result demonstrated that the silencing of CD164 increased the levels of PTEN and p53, whereas the level of p-AKT was decreased by transduction of CD164 shRNA. CD164 may induce the apoptosis of U87 cell by down-regulating PTEN/PI3K/AKT signal pathway in vitro, providing a novel ideal to improving the diagnosis and treatment of glioma patients.


Key words: CD164, U87, PTEN, apoptosis.


Tu and Zheng