Sansong Chen1, Qifu Wang1, Xuefei Shao1, Guangfu Di1, Yi Dai1, Xiaochun Jiang2, Limin Cheng3. 1. Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No.2 Zheshan Road, Wuhu, 241001, Anhui, China. 2. Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No.2 Zheshan Road, Wuhu, 241001, Anhui, China. Electronic address: jiangxiaochun2001@hotmail.com. 3. Central Laboratory of Microscopic Morphology, School of Preclinical Medicine, Wannan Medical College, Wuhu, 241002, Anhui, China. Electronic address: 630336548@qq.com.
Abstract
BACKGROUND: Glioma is the most common malignancy in brain carcinoma with poor prognosis due to the lack of understanding of the mechanism underlying the disease. γ-interferon-inducible lysosomal thiol reductase (GILT) plays a critical role in the process of antigen processing. However, the role of GILT in the tumorigenesis of glioma remains unknown. MATERIALS AND METHODS: The expression of GILT was analyzed by bioinformatics using the public database and by qPCR in three human glioma cell lines. Cell growth and viability were determined by Celigo and MTT assays, while cell cycle arrest and apoptosis were determined using flow cytometry. Giemsa staining was used to analyze the colony formation, while cell motility was assessed using transwell migration and invasion assays, as well as, using tumor growth in nude mice. RESULTS: GILT was highly expressed as observed in the public database on human gliomas and two human glioma cell lines, U373MG and U87MG cells. The downregulation of GILT by lentiviral-mediated silencing inhibits the cell growth, colony formation, and migration but promotes apoptosis and results in cell cycle arrest at the G0/G1 phase in the U373MG cells. Also, the knockdown of GILT inhibits tumor growth in vivo. CONCLUSION: Elevated GILT is positively associated with glioma progression. GILT silencing suppresses cell proliferation, colony formation, migration, and tumor growth, and induces apoptosis and cell cycle arrest. GILT may serve as a potential target for the treatment of glioma.
BACKGROUND:Glioma is the most common malignancy in brain carcinoma with poor prognosis due to the lack of understanding of the mechanism underlying the disease. γ-interferon-inducible lysosomal thiol reductase (GILT) plays a critical role in the process of antigen processing. However, the role of GILT in the tumorigenesis of glioma remains unknown. MATERIALS AND METHODS: The expression of GILT was analyzed by bioinformatics using the public database and by qPCR in three humanglioma cell lines. Cell growth and viability were determined by Celigo and MTT assays, while cell cycle arrest and apoptosis were determined using flow cytometry. Giemsa staining was used to analyze the colony formation, while cell motility was assessed using transwell migration and invasion assays, as well as, using tumor growth in nude mice. RESULTS:GILT was highly expressed as observed in the public database on humangliomas and two humanglioma cell lines, U373MG and U87MG cells. The downregulation of GILT by lentiviral-mediated silencing inhibits the cell growth, colony formation, and migration but promotes apoptosis and results in cell cycle arrest at the G0/G1 phase in the U373MG cells. Also, the knockdown of GILT inhibits tumor growth in vivo. CONCLUSION: Elevated GILT is positively associated with glioma progression. GILT silencing suppresses cell proliferation, colony formation, migration, and tumor growth, and induces apoptosis and cell cycle arrest. GILT may serve as a potential target for the treatment of glioma.