Protein phosphatase 4 catalytic subunit is overexpressed in glioma and promotes glioma cell proliferation and invasion
Protein phosphatase 4 catalytic subunit (PP4C) has been identified to be overexpressed in various solid cancers. However, to date, the role of PP4C in glioma remains elusive. In the present study, we aimed to detect PP4C expression in glioma patients and explore its function in glioma and prognostic significance in patients with glioma. The expression levels of PP4C mRNA and protein in 30 glioma tissue specimens and 10 non-cancerous brain tissue specimens were detected by qRT-PCR and Western blot analysis. Moreover, immunohistochemistry was performed to assess PP4C expression in 120 glioma patients. The effects of siRNA-mediated PP4C silencing on the proliferation, migration, and invasion of U251 and U87 glioma cells were assessed. We found that PP4C was upregulated in glioma tissue at both mRNA and protein levels compared with non-cancerous brain tissue. Univariate and multivariate analyses indicated that high PP4C expression was an independent prognostic factor for poor survival of glioma patients. Knockdown of PP4C reduced the proliferation, migration, and invasion of U251 and U87 cells. In conclusion, our findings suggest that PP4C plays an oncogenic role in glioma development and progression and might serve as a prognostic biomarker as well as a potential therapeutic target for glioma.
KeywordsGlioma PP4C Prognosis Biomarker
The project was supported by the National Natural Science Foundation of China (No. 81372721) and Natural Science Foundation of Shandong Province (No. ZR2013HM011).
Compliance with ethical standards
This study was approved by Ethics Committee of Liaocheng People’s Hospital and Qilu Hospital. Written informed consent was obtained from all the patients.
Conflicts of interest
- 7.Theobald B, Bonness K, Musiyenko A, Andrews JF, Urban G, Huang X, et al. Suppression of ser/thr phosphatase 4 (PP4C/PPP4C) mimics a novel post-mitotic action of fostriecin, producing mitotic slippage followed by tetraploid cell death. Molecular cancer research : MCR. 2013;11:845–55.CrossRefPubMedPubMedCentralGoogle Scholar