11 October 2018 : Laboratory Research
Effects of Enhancer of Zeste Homolog 2 (EZH2) Expression on Brain Glioma Cell Proliferation and TumorigenesisTianci Cheng1BDF, Yinghui Xu1ACEG*
Med Sci Monit 2018; 24: LBR7249-7255
BACKGROUND: Brain glioma is a type of common primary intracranial malignant tumor, the prognosis of which is frequently unfavorable. Enhancer of zeste homolog 2 (EZH2) belongs to poly-sulfur protein family and can mediate cell proliferation and differentiation via the modulation of various genes expressions. In addition, it is further related with occurrence and metastasis of malignant tumors. This study investigated the effect of EZH2 expression on proliferation and tumorigenesis of brain glioma cells.
MATERIAL AND METHODS: Glioma tumor tissues were collected from 3 patients who received surgery, and the glioma stem cells were then separated, cultured, and identified by flow cytometry. RNA interference approach was used to suppress EZH2 expression, which was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). Clonal formation assay analyzed the change of cell proliferation potency. The effect on tumorigenesis potency of glioma stem cells was determined by mouse transplantation assay. Western blot investigated the effect of EZH2 on levels of oncogenes such as HER-2, c-myc, PI3K, and Akt.
RESULTS: Flow cytometry revealed cancer stem cells in glioma tissues took up 39.4%, and qRT-PCR showed that EZH2 expression was decreased by 72% after the treatment of RNA interference in glioma cells (P<0.05). Both cell clonal formation and xenograft assays showed that the downregulation of EZH2 inhibited glioma cell proliferation (P<0.05) and weakened tumorigenesis potency (P<0.05). Western blot results showed that the reduction of EZH2 also suppressed expressions of oncogenes including c-myc and Akt (P<0.05).
CONCLUSIONS: Our data demonstrated that in brain glioma cells, the decrease of EZH2 level could suppress cell proliferation and tumorigenesis potency, and meanwhile inhibit the expressions of oncogenes including c-myc and Akt.
Keywords: Cells, Glioma
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