Original Article
CENPE promotes glioblastomas proliferation by directly binding to WEE1
Abstract
Background: Glioblastoma (GBM) is one of the most lethal tumors. Even though radiotherapy and chemotherapy have been greatly developed, the survival of patients with GBM is still only about 16 months.
Methods: In this assay, centromere protein E (CENPE) expression levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) assays. 5-ethynyl-2’-deoxyuridine (EDU) assay was used to assess the effect of CENPE on cell proliferation. The propidium iodide (PI) method was used to detect the cell cycle.
Results: CENPE expression was increased in GBM tissues and was associated with clinical stage and unfavorable overall survival in glioma patients. Inhibition of CENPE expression resulted in proliferation inhibition of U251 and U87 cell. Cell cycle assay showed that CENPE mainly regulates the G0–G1 and G2/M phase transitions. Then, we found that CENPE regulated the proliferation of GBM mainly through WEE1 G2 checkpoint kinase (WEE1) pathway and can bind to WEE1.
Conclusions: CENPE promotes GBM proliferation through WEE1 pathway and binding to WEE1.
Methods: In this assay, centromere protein E (CENPE) expression levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) assays. 5-ethynyl-2’-deoxyuridine (EDU) assay was used to assess the effect of CENPE on cell proliferation. The propidium iodide (PI) method was used to detect the cell cycle.
Results: CENPE expression was increased in GBM tissues and was associated with clinical stage and unfavorable overall survival in glioma patients. Inhibition of CENPE expression resulted in proliferation inhibition of U251 and U87 cell. Cell cycle assay showed that CENPE mainly regulates the G0–G1 and G2/M phase transitions. Then, we found that CENPE regulated the proliferation of GBM mainly through WEE1 G2 checkpoint kinase (WEE1) pathway and can bind to WEE1.
Conclusions: CENPE promotes GBM proliferation through WEE1 pathway and binding to WEE1.
