Early growth response 1 promoted the invasion of glioblastoma multiforme by elevating HMGB1

被引:8
作者
DU, Kai [1 ]
Wu, Xiaoyou [2 ]
Ji, Xiaofei [2 ]
Liang, Nan [3 ]
LI, Zheng [3 ]
机构
[1] Yidu Cent Hosp Weifang, Dept Neurosurg, Weifang, Peoples R China
[2] Yidu Cent Hosp Weifang, Dept Pediat, Weifang, Peoples R China
[3] First Med Univ, Dept Neurosurg, Hosp Shandong 2, 706 Taishan Rd, Tai An 271000, Shandong, Peoples R China
关键词
Glioblastoma; Early growth response protein 1; Prognosis; POOR-PROGNOSIS; TUMOR-SUPPRESSOR; DOWN-REGULATION; EXPRESSION; CANCER; CELLS; ACTIVATION; PTEN; TRANSCRIPTION; MUTATIONS;
D O I
10.23736/S0390-5616.20.05107-3
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
BACKGROUND: Glioblastoma multiforme (GBM) is the most common and deadly glioma subtype. Early growth response 1 (EGR1) participates in the progression of several cancer types, but the expression and function of EGR1 in GBM was rarely investigated. METHODS: The expressions of EGR1 in GBM were detected with qRT-PCR and immunohistochemistry in 12 pairs of fresh GBM tissues and 116 paraffin-embedded specimens. The patients were divided into high and low EGR1 groups according to the IHC score of EGR1, and the prognostic significances of different groups were evaluated with univariate and multivariate analyses. With in-vitro experiments, we assessed the role of EGR1 in the proliferation and invasion of GBM cells. RESULTS: In our study, EGR1 was up-regulated in GBM tissues compared with tumor-adjacent normal tissues. High expression of EGR1 or HMGB1 were unfavorable prognostic biomarkers of GBM. Coexpression of EGR1 and HMGB1 could predict the prognosis of GBM more sensitively. EGR1 facilitated the proliferation and invasion of GBM cells. Moreover, EGR1 promoted the invasion, instead of proliferation, of GBM cells by elevating the expression of HMGB1. CONCLUSIONS: ERG1 was a prognostic biomarker of GBM, and ERG1 and HMGB1 synergistically could predict the GBM prognosis more precisely. ERG1 could promote GBM cell invasion by inducing HMGB1 expression.
引用
收藏
页码:422 / 430
页数:9
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