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胶质瘤中MICALL2的表达与临床意义

隋馨瑶 高静

中国医科大学学报2025,Vol.54Issue(7):590-594,5.
中国医科大学学报2025,Vol.54Issue(7):590-594,5.DOI:10.12007/j.issn.0258-4646.2025.07.003

胶质瘤中MICALL2的表达与临床意义

Clinical implications and the expression of MICALL2 in glioma

隋馨瑶 1高静2

作者信息

  • 1. 锦州医科大学基础医学院病理生理教研室,辽宁 锦州 121000
  • 2. 锦州医科大学附属第一医院超声科,辽宁 锦州 121000
  • 折叠

摘要

Abstract

Objective To investigate the expression of MICALL2 in glioma,analyze its correlation with clinicopathological characteri-stics and prognosis in patients with glioma,and explore the potential biological role of MICALL2 in glioma.Methods Immunohisto-chemical staining of glioma tissue chips was performed to compare the differential expression of MICALL2 in glioma and normal brain tissues.Public databases,including The Cancer Genome Atlas(TCGA),Gene Expression Profiling Interactive Analysis(GEPIA),and Gene Expression Database of Normal and Tumor Tissues 2(GENT2),were used to assess the association between MICALL2 expression and prognosis in patients with glioma.Gene set enrichment analysis(GSEA)was conducted to identify the differentially expressed genes associated with MICALL2 in low-grade gliomas and to infer their biological functions.Results The expression of MICALL2 was higher in glioma tissues than in normal brain tissues(P<0.001).MICALL2 expression correlated with TNM staging(P<0.01)and tumor size(P<0.01)in patients with gliomas.Survival analysis indicated that MICALL2 may be an influencing factor of the prognosis in patients with glioma.GSEA enrichment analysis revealed that MICALL2 may be involved in the regulation of intercellular adhesion pathways in gliomas.Conclusion MICALL2 is overexpressed in glioma tissues and may negatively affect patient prognosis,indicating its potential as a therapeutic target and prognostic biomarker for gliomas.

关键词

胶质瘤/MIACLL2/临床意义/预后

Key words

glioma/MICALL2/clinical implication/prognosis

分类

医药卫生

引用本文复制引用

隋馨瑶,高静..胶质瘤中MICALL2的表达与临床意义[J].中国医科大学学报,2025,54(7):590-594,5.

基金项目

辽宁省自然科学基金(2022-MS-392) (2022-MS-392)

中国医科大学学报

OA北大核心

0258-4646

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