STC2通过调节ITGB2调控胶质瘤细胞的增殖、迁移和糖酵解。

IF 3.2 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Zefeng Wei, Dengfeng Ge, Jie Bu, Xuenan Wang, Tao Zhong, Xiaoxiao Gongye, Bin Zhang, Feng Yan, Chunyan He, Runhan Guo, Jiayi Li, Zhenzhen Jin
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引用次数: 0

摘要

胶质瘤是一种常见的侵袭性原发性恶性脑肿瘤。然而,胶质瘤的发生机制尚未得到很好的揭示。在本研究中,我们打算检测STC2在胶质瘤中的功能及其相关机制。使用基因表达谱交互分析数据库检测胶质瘤样本中STC2和ITGB2的表达,以及STC2与其他基因的关系。联合免疫沉淀法证实STC2与ITGB2的关系。通过细胞计数试剂盒-8、集落形成、transwell、ELISA和western blot检测胶质瘤细胞的生物学功能。我们发现STC2在胶质瘤样本和细胞系中高度表达。STC2的下调抑制了细胞的增殖、侵袭、迁移和糖酵解。进一步分析表明ITGB2与STC2之间存在相互作用,并参与STC2调控的增殖、侵袭、迁移和糖酵解。总之,我们的数据为理解STC2的调控机制提供了新的见解,并表明STC2/ITGB2轴可能是胶质瘤的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
STC2 regulates the proliferation, migration and glycolysis of glioma cells through modulating ITGB2.

Glioma is a common and aggressive primary malignant brain tumor. However, the progression mechanism of glioma has not been well revealed. In this study, we intend to detect the function and related mechanism of STC2 in glioma. Gene Expression Profiling Interactive Analysis database was used to detect STC2 and ITGB2 expression in glioma samples, as well as the relationship between STC2 and other genes. The relationship between STC2 and ITGB2 was confirmed by co-immunoprecipitation assay. The biology function of glioma cells was determined by cell counting kit-8, colony formation, transwell, ELISA and western blot assays. We discovered that STC2 was highly expressed in glioma samples and cell lines. Knocked down of STC2 inhibited cell proliferation, invasion, migration and glycolysis. Further analysis demonstrated the interaction between ITGB2 and STC2 as well as its involvement in STC2-regulated proliferation, invasion, migration and glycolysis. In summary, our data afforded novel insights into understanding the regulatory mechanism of STC2 and suggested that the STC2/ITGB2 axis might be a potential therapeutic target for glioma.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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