昆明医科大学学报2024，Vol.45Issue(5)：29-36,8.DOI:10.12259/j.issn.2095-610X.S20240505
过表达三结构域蛋白48调控p-ERK1/2抑制胶质瘤生长的作用机制
Researches on the Mechanism of Overexpression of Tripartite Motif Protein 48 Regulating p-ERK1/2 to Inhibit Glioma Growth
摘要
Abstract
Objective To investigate the impact of TRIM48 overexpression on glioma and explore the underlying mechanism.Methods Twelve nude mice were randomly assigned into two groups:one inoculated with U87 glioma cells stably overexpressing TRIM48(oeTRIM48 group)and the other with the control cell line(Vector group).Tumor volume was measured every 3 days post-inoculation,and after 4 weeks,the tumors were excised and weighed.Tumor tissues underwent hematoxylin and eosin(H&E)staining,and Ki-67 expression was assessed using immunofluorescence.Additionally,the expressions of TRIM48,ERK1/2,and phosphorylated ERK1/2(p-ERK1/2)in the tumors of nude mice and human glioma tissue arrays were analyzed through Western blot and immunohistochemistry respectively.Results Compared to the Vector group,the oeTRIM48 group exhibited significantly reduced tumor volume and weight(P<0.0001).H&E staining indicated a decrease in nuclei and mitotic count in the oeTRIM48 group.Furthermore,Ki-67 expression was significantly lower in the oeTRIM48 group than that in the Vector group(P<0.0001).The oeTRIM48 group also showed a significantly lower expression of p-ERK1/2 protein compared to the Vector group(P<0.01).Immunohistochemistry on tissue microarrays revealed the high expression of TRIM48 and low expression of p-ERK1/2 in adjacent non-tumoral tissues,with the opposite pattern observed in tumor tissues.Conclusion Overexpression of TRIM48 inhibits the growth and proliferation of glioma,potentially through modulation of the ERK1/2 signaling pathway.关键词
TRIM48/胶质瘤/ERK1/2Key words
TRIM48/Glioma/ERK1/2分类
医药卫生引用本文复制引用
姜右川,余妍,赵国,李世存,丁鹏..过表达三结构域蛋白48调控p-ERK1/2抑制胶质瘤生长的作用机制[J].昆明医科大学学报,2024,45(5):29-36,8.基金项目
云南省科技厅-昆明医科大学应用基础研究联合专项重点基金资助项目(202001AY070001-160) （202001AY070001-160）
云南省卫生高层次人才专项基金资助项目(L-2019020) （L-2019020）
