Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No.2 Zheshan Road, Wuhu, 241001, Anhui, China.
Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, No.2 Zheshan Road, Wuhu, 241001, Anhui, China.
Biochem Biophys Res Commun. 2019 Jan 29;509(1):182-187. doi: 10.1016/j.bbrc.2018.12.099. Epub 2018 Dec 23.
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.
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.
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.
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.
由于对疾病发病机制缺乏了解，神经胶质瘤是脑癌中最常见的恶性肿瘤，预后较差。γ-干扰素诱导的溶酶体硫醇还原酶（GILT）在抗原加工过程中发挥关键作用。然而，GILT 在神经胶质瘤的发生发展中的作用尚不清楚。
使用公共数据库和 qPCR 分析三种人神经胶质瘤细胞系中 GILT 的表达。通过 Celigo 和 MTT 测定法测定细胞生长和活力，通过流式细胞术测定细胞周期停滞和细胞凋亡。吉姆萨染色分析集落形成，通过 Transwell 迁移和侵袭测定以及裸鼠肿瘤生长评估细胞迁移。
在人类神经胶质瘤和两种人神经胶质瘤细胞系 U373MG 和 U87MG 中，公共数据库观察到 GILT 高表达。通过慢病毒介导的沉默下调 GILT 抑制细胞生长、集落形成和迁移，但促进细胞凋亡，并导致 U373MG 细胞周期停滞在 G0/G1 期。此外，GILT 的敲低抑制体内肿瘤生长。
GILT 升高与神经胶质瘤进展呈正相关。GILT 沉默抑制细胞增殖、集落形成、迁移和肿瘤生长，并诱导细胞凋亡和细胞周期停滞。GILT 可能成为神经胶质瘤治疗的潜在靶点。
