Repression of PCGF1 Decreases the Proliferation of Glioblastoma Cells in Association with Inactivation of c-Myc Signaling Pathway
Received 13 October 2019
Accepted for publication 12 December 2019
Published 9 January 2020 Volume 2020:13 Pages 253—261
Checked for plagiarism Yes
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Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Nicola Silvestris
Rui Yan,1,* Fengmei Cui,2,* Lijin Dong,3,* Yong Liu,4 Xuewei Chen,5 Rong Fan4
1Department of Thoracic Surgery, The Third Medical Center, Chinese People’s Liberation Army General Hospital, Beijing 100039, People’s Republic of China; 2Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou 215123, People’s Republic of China; 3Editorial Department, Logistic University of Chinese People’s Armed Police Force, Tianjin 300309, People’s Republic of China; 4Central Laboratory, Xi Qing Hospital, Tianjin 300380, People’s Republic of China; 5Department of Operational Medicine, Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xuewei Chen; Rong Fan Email firstname.lastname@example.org; email@example.com
Purpose: Glioblastoma (GBM) is the most common primary brain tumor with a poor therapeutic outcome. Polycomb group factor 1 (PCGF1), a member of the PcG (Polycomb group) family, is highly expressed in the developing nervous system of mice. However, the function and the mechanism of PCGF1 in GBM proliferation still remain unclear.
Methods: Knockdown of PCGF1 was performed in U87 GBM cell by shRNA strategy via lentivirus vector. MTT assay, colony formation assays, and flow cytometry were used to measure the properties of cell proliferation and cell cycle distribution, respectively. GeneChip analysis was performed to identify the downstream effector molecules. Rescue assay was constructed to verify the screening results.
Results: We first found that knockdown of PCGF1 led to the inhibition of U87 cells proliferation and decreased colony formation ability. The data from GeneChip expression profiling and Ingenuity Pathway Analysis (IPA) indicated that many of the altered gene cells are associated with the cell proliferation control pathways. We have further confirmed the suppression of AKT/GSK3β/c-Myc/cyclinD1 expressions by Western blotting analysis. The over-expression of c-Myc could partly restore the attenuated proliferation ability caused by knockdown of PCGF1.
Conclusion: All the above evidences suggested that PCGF1 might be closely associated with tumorigenesis and progression of glioblastoma (GBM), in which process the oncoprotein c-Myc may participate. PCGF1 could thus be a potential therapeutic target for the treatment of glioblastoma (GBM).
Keywords: glioblastoma, GBM, PCGF1, cell proliferation, polycomb group
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