BOC靶向SMO调控Hedgehog通路,促进胶质瘤细胞的增殖、迁移和侵袭

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发表时间:2025-01-22 16:51

202410月,呼和浩特**医院医学检验科;内蒙古农业大学生命科学学院;内蒙古自治区人民医院神经内科 (Department of Medical Laboratory, Huhhot First Hospital, Hohhot, Inner Mongolia 010020, China b College of Life Sciences, Inner Mongolia Agricultural University, Hohhot, Inner Mongolia 010018, China c Department of Neurology, Inner Mongolia Autonomous Region Peoples Hospital, Hohhot, Inner Mongolia 010017, China) Bin Liu老师研究团队在Brain Research Bulletin上发表论文:

BOC targets SMO to regulate the Hedgehog pathway and promote proliferation, migration, and invasion of glioma cells


BOC靶向SMO调控Hedgehog通路,促进胶质瘤细胞的增殖、迁移和侵袭


Abstract

The purpose of this study was to investigate the effects of BOC on glioblastoma cells and its underlying mechanisms. In vitro, BOC-knockdown was performed in glioma cell lines. CCK-8 and Transwell were used to assess the impact of BOC on the viability, invasion, and migration of gliobma cells. RNA-seq technology was employed to analyze the differential gene expression between BOC-knockdown glioma cells and the control group, and qRT-PCR was used to validate the expression of downstream differential genes. SMO-overexpression was performed to investigate the effects of SMO on glioma cells. A BOC-knockdown mouse subcutaneous tumor model was to verify the effects of BOC on mouse tumors. Tissue microarray technology was used to detect the expression of BOC and SMO in samples of normal human brain tissue and glioma tissue. In vitro, BOC-knockdown inhibited the viability, invasion, and migration of glioma cells, as well as downregulated the expression of downstream differential genes SMO, EGFR, HRAS, and MRAS. Conversely, SMO-overexpression upregulated the viability, invasion, and migration abilities of BOC-knockdown cells. In vivo, BOC-knockdown suppressed tumor growth in mice and downregulated the expression of downstream differential genes SMO, EGFR, HRAS, and MRAS. Tissue microarray results showed that both BOC and SMO were highly expressed in glioma tissues. BOC is aberrantly overexpressed in glioma patients and promotes glioma development. Mechanistically, BOC activates the Hedgehog (Hh) and RAS signaling pathways by upregulating the expression of SMO, EGFR, HRAS, and MRAS, thereby facilitating the Proliferation, invasion and migration of glioma cells.

摘要:

本研究的目的是探讨中银对胶质母细胞瘤细胞的影响及其潜在机制。体外,在胶质瘤细胞系中进行了boc敲除。CCK-8和Transwell用于评估中银对胶质瘤细胞活力、侵袭和迁移的影响。采用RNA-seq技术分析boc敲除胶质瘤细胞与对照组的差异基因表达,采用qRT-PCR验证下游差异基因的表达。通过SMO过表达研究SMO对胶质瘤细胞的影响。建立BOC敲除小鼠皮下肿瘤模型,验证BOC对小鼠肿瘤的作用。采用组织微阵列技术检测正常人脑组织和胶质瘤组织中BOC和SMO的表达。在体外实验中,boc -敲低抑制胶质瘤细胞的活力、侵袭和迁移,下调下游差异基因SMO、EGFR、HRAS和MRAS的表达。相反,smo -过表达上调了boc -敲低细胞的活力、侵袭和迁移能力。在体内,敲低boc抑制小鼠肿瘤生长,下调下游差异基因SMO、EGFR、HRAS和MRAS的表达。组织微阵列结果显示,在胶质瘤组织中,BOC和SMO均高表达。BOC在胶质瘤患者中异常过表达并促进胶质瘤的发展。在机制上,BOC通过上调SMO、EGFR、HRAS和MRAS的表达激活Hedgehog (Hh)和RAS信号通路,从而促进胶质瘤细胞的增殖、侵袭和迁移。


该论文中,U251细胞(人胶质瘤细胞)和U87MG细胞(人胶质瘤多形性细胞)HEB细胞(人星形胶质细胞)和A172细胞(人胶质瘤细胞)的体外培养是使用Ausbian特级胎牛血清完成的欲了解或购买Ausbian特级胎牛血清可以联系北京缔一生物400-166-8600.



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