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：
目的探讨BOC对胶质母细胞瘤细胞的作用及其机制。体外，在神经胶质瘤细胞系中进行BOC敲除。CCK-8和Transwell用于评估BOC对生存能力的影响，入侵,和神经胶质细胞的迁移。采用RNA-seq技术分析BOC敲低胶质瘤细胞与对照组的差异基因表达,qRT-PCR用于验证下游差异基因的表达。进行SMO过表达以研究SMO对神经胶质瘤细胞的影响。BOC敲低小鼠皮下肿瘤模型用于验证BOC对小鼠肿瘤的作用。组织芯片技术用于检测正常人脑组织和胶质瘤组织中BOC和SMO的表达。体外，BOC敲除抑制了生存能力，入侵,和神经胶质瘤细胞的迁移，以及下调下游差异基因SMO的表达，EGFR,HRAS,和MRAS。相反，SMO过表达上调了生存力，入侵,和BOC敲低细胞的迁移能力。在体内,BOC敲低抑制小鼠肿瘤生长，下调下游差异基因SMO的表达，EGFR,HRAS,和MRAS。组织芯片结果显示BOC和SMO在胶质瘤组织中均高表达。BOC在神经胶质瘤患者中异常过度表达并促进神经胶质瘤的发展。机械上,BOC通过上调SMO的表达激活Hedgehog(Hh)和RAS信号通路,EGFR,HRAS,还有MRAS,从而促进扩散，胶质瘤细胞的侵袭和迁移。
