Department of Medical Laboratory, Huhhot First Hospital, Hohhot, Inner Mongolia 010020, China.
College of Life Sciences, Inner Mongolia Agricultural University, Hohhot, Inner Mongolia 010018, China.
Brain Res Bull. 2024 Oct 1;216:111037. doi: 10.1016/j.brainresbull.2024.111037. Epub 2024 Jul 30.
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.
本研究旨在探讨 BOC 对神经胶质瘤细胞的影响及其作用机制。体外实验中，在神经胶质瘤细胞系中敲低 BOC 的表达。CCK-8 和 Transwell 实验用于评估 BOC 对神经胶质瘤细胞活力、侵袭和迁移的影响。RNA-seq 技术用于分析 BOC 敲低神经胶质瘤细胞与对照组之间差异基因的表达，qRT-PCR 用于验证下游差异基因的表达。SMO 过表达用于研究 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 对小鼠肿瘤的影响。组织微阵列技术用于检测正常脑组织和神经胶质瘤组织样本中 BOC 和 SMO 的表达。体外实验中，BOC 敲低抑制神经胶质瘤细胞的活力、侵袭和迁移，并下调下游差异基因 SMO、EGFR、HRAS 和 MRAS 的表达。相反，SMO 过表达上调 BOC 敲低细胞的活力、侵袭和迁移能力。体内实验中，BOC 敲低抑制小鼠肿瘤生长并下调下游差异基因 SMO、EGFR、HRAS 和 MRAS 的表达。组织微阵列结果表明，BOC 和 SMO 在神经胶质瘤组织中均高度表达。BOC 在神经胶质瘤患者中异常过表达，并促进神经胶质瘤的发展。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，从而促进神经胶质瘤细胞的增殖、侵袭和迁移。
