Limin Cheng1, Xuefei Shao2, Qifu Wang2, Xiaochun Jiang2, Yi Dai3, Sansong Chen4. 1. Morphology Experiment & Training Center, School of Preclinical Medicine, Wannan Medical College, Wuhu 241002, Anhui, China. 2. Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No. 2 Zheshan Road, Wuhu 241001, Anhui, China. 3. Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No. 2 Zheshan Road, Wuhu 241001, Anhui, China. Electronic address: yjsyy0775@163.com. 4. Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No. 2 Zheshan Road, Wuhu 241001, Anhui, China. Electronic address: mansion1006@163.com.
Abstract
BACKGROUND: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: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. MATERIALS AND METHODS:AEBP1 expression was analyzed by bioinformatics using the public database and by qPCR and western blotting in humanglioma 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. RESULTS:AEBP1 is highly expressed in humangliomas. Lipofectamine 3000-mediated siRNA transfection stably and efficiently suppressed AEBP1 mRNA and protein expression in humanglioma 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. CONCLUSION: 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.