Morphology Experiment & Training Center, School of Preclinical Medicine, Wannan Medical College, Wuhu 241002, Anhui, China.
Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No. 2 Zheshan Road, Wuhu 241001, Anhui, China.
Pathol Res Pract. 2020 Feb;216(2):152790. doi: 10.1016/j.prp.2019.152790. Epub 2019 Dec 17.
Glioma is the most common primary malignant tumor with poor prognosis due to the lack of understanding the mechanism underlying the disease and the early diagnosis indexs. It is necessary to identify molecular signatures for predicting the overall prognosis of glioma. Adipocyte enhancer binding protein1 (AEBP1) acts as a transcriptional repressor and plays a role in adipogenesis and smooth muscle cell differentiation. However, its role in glioma remains unclear.
AEBP1 expression was analyzed by bioinformatics using the public database and by qPCR and western blotting in human glioma tissues. AEBP1 downregulation was performed by lipofectamine3000-mediated siRNA transfection. Cell proliferation and invasion were determined by cell counting kit-8 and transwell assays, while early cell apoptosis was determined by flow cytometry. The proteins of downstream NF-κB signaling pathway were determined by western blotting.
AEBP1 is highly expressed in human gliomas. Lipofectamine 3000-mediated siRNA transfection stably and efficiently suppressed AEBP1 mRNA and protein expression in human glioma cells. AEBP1 downregulation inhibited cell proliferation and invasion, but promoted early cell apoptosis. Also, AEBP1 knockdown in glioma cells decreased the expression of NF-κB1. Furthermore, the downstream of NF-κB signaling pathway, Bax, caspase-3 are increased, while MMP2 and Bcl-2 are decreased in glioma cells.
Elevated AEBP1 is positively associated with poor prognosis of glioma. AEBP1 downregulation suppressed cell proliferation and invasion, but promoted early cell apoptosis. AEBP1 downregulation suppressed the cell proliferation and invasion may by inhibiting the NF-κB signaling pathway.
由于缺乏对疾病机制和早期诊断指标的了解,神经胶质瘤是预后最差的最常见原发性恶性肿瘤。有必要确定分子特征以预测神经胶质瘤的总体预后。脂肪细胞增强结合蛋白 1(AEBP1)作为转录抑制因子,在脂肪生成和平滑肌细胞分化中发挥作用。然而,其在神经胶质瘤中的作用尚不清楚。
使用公共数据库和 qPCR 和 Western blot 分析人神经胶质瘤组织中的 AEBP1 表达。通过脂质体 3000 介导的 siRNA 转染下调 AEBP1。通过细胞计数试剂盒-8 和 Transwell 测定法测定细胞增殖和侵袭,通过流式细胞术测定早期细胞凋亡。通过 Western blot 测定 NF-κB 信号通路的下游蛋白。
AEBP1 在人神经胶质瘤中高表达。脂质体 3000 介导的 siRNA 转染稳定且有效地抑制了人神经胶质瘤细胞中 AEBP1 的 mRNA 和蛋白表达。AEBP1 下调抑制细胞增殖和侵袭,但促进早期细胞凋亡。此外,神经胶质瘤细胞中 AEBP1 的敲低降低了 NF-κB1 的表达。此外,下游的 NF-κB 信号通路,Bax、caspase-3 增加,而 MMP2 和 Bcl-2 在神经胶质瘤细胞中减少。
AEBP1 的升高与神经胶质瘤的不良预后呈正相关。AEBP1 下调抑制细胞增殖和侵袭,但促进早期细胞凋亡。AEBP1 下调抑制细胞增殖和侵袭可能通过抑制 NF-κB 信号通路。