PTEN公司
基因敲除
胶质瘤
蛋白激酶B
癌症研究
PI3K/AKT/mTOR通路
癌变
细胞生长
活力测定
生物
细胞迁移
信号转导
细胞
细胞生物学
细胞凋亡
癌症
生物化学
遗传学
作者
Hengzhu Zhang,Xiaofeng Hou,ZhengXiong Kou
出处
期刊:Journal of Environmental Pathology Toxicology and Oncology
[Begell House Inc.]
日期:2023-01-01
卷期号:42 (2): 1-9
标识
DOI:10.1615/jenvironpatholtoxicoloncol.2022044068
摘要
Dysregulation of pseudogene expression is closely related to the progression of various cancers, including glioma. Proliferation-associated 2G4 pseudogene 4 (<i>PA2G4P4</i>) could affect cell viability and apoptosis of glioma cells. However, the specific regulatory mechanism of PA2G4P4 is not clear. In this paper, we found that PA2G4P4 overexpres-sion promoted glioma cell proliferation, migration and cell cycle progression, whereas PA2G4P4 knockdown inhibited cancer progression. Knockdown of PA2G4P4 also suppressed the tumorigenesis of glioma cells <i>in vivo</i>. Furthermore, knockdown of PA2G4 after overexpression of PA2G4P4 decreased the cell viability and migration ability to normal level. The protein level of a tumor suppressor gene phosphatase and tensing homolog (PTEN) was greatly decreased in U87 cells after PA2G4P4 overexpression, while increased after PA2G4 knockdown; on the contrary, the protein levels of P-AKT and P-S6 were obviously induced in U87 cells after PA2G4P4 overexpression, and decreased after PA2G4 knockdown. The cell ability, colony formation ability and cell migration ability were all recovered to normal level by adding an AKT inhibitor MK2206 to the glioma cells, which were induced by PA2G4P4 overexpression. Our results revealed that PA2G4P4 could regulate glioma cell proliferation and migration through PTEN/AKT/mTOR signaling pathway by targeting PA2G4 gene. PA2G4P4 may become a target for glioma treatment.
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