Depletion of thymopoietin inhibits proliferation and induces cell cycle arrest-apoptosis in glioblastoma cellsReport as inadecuate




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World Journal of Surgical Oncology

, 14:267

First Online: 19 October 2016Received: 01 April 2016Accepted: 04 October 2016

Abstract

BackgroundGlioblastoma GBM is the most malignant nervous system tumor with an almost 100 % recurrence rate. Thymopoietin TMPO has been demonstrated to be upregulated in various tumors, including lung cancer, breast cancer, and so on, but its role in GBM has not been reported. This study was aimed to determine the role of TMPO in GBM.

MethodsPublicly available Oncomine dataset analysis was used to explore the expression level of TMPO in GBM specimens. Then the expression of TMPO was knocked down in GBM cells using lentiviral system, and the knockdown efficacy was further validated by real-time quantitative PCR and western blot analysis. Furthermore, the effects of TMPO silencing on GBM cell proliferation and apoptosis were examined by MTT, colony formation, and flow cytometry analysis. Meanwhile, the expression of apoptotic markers caspase-3 and polyADP-ribose polymerase PARP were investigated by western blot analysis.

ResultsThis study observed that the expression of TMPO in GBM specimens was remarkably higher than that in normal brain specimens. Moreover, knockdown of TMPO could significantly inhibit cell proliferation and arrest cell cycle progression at the G2-M phase. It also found that TMPO knockdown promoted cell apoptosis by upregulation of the cleavage of caspase-3 and PARP protein levels which are the markers of apoptosis.

ConclusionsThe results suggested TMPO might be a novel therapeutic target for GBM.

KeywordsTMPO Glioblastoma Cell proliferation Apoptosis  Download fulltext PDF



Author: Lin Zhang - Gan Wang - Shiwen Chen - Jun Ding - Shiming Ju - Heli Cao - Hengli Tian

Source: https://link.springer.com/



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