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BOC靶向SMO調控Hedgehog通路，促進膠質瘤細胞的增殖、遷移和侵襲

二維碼

發表時間：2025-01-22 16:51

2024年10月，呼和浩特**醫院醫學檢驗科；內蒙古農業大學生命科學學院；內蒙古自治區人民醫院神經內科 (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 People’s Hospital, Hohhot, Inner Mongolia 010017, China) Bin Liu老師研究團隊在《Brain Research Bulletin》上發表論文：

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

“BOC靶向SMO調控Hedgehog通路，促進膠質瘤細胞的增殖、遷移和侵襲”

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：

本研究的目的是探討中銀對膠質母細胞瘤細胞的影響及其潛在機制。體外，在膠質瘤細胞系中進行了boc敲除。CCK-8和Transwell用于評估中銀對膠質瘤細胞活力、侵襲和遷移的影響。采用RNA-seq技術分析boc敲除膠質瘤細胞與對照組的差異基因表達，采用qRT-PCR驗證下游差異基因的表達。通過SMO過表達研究SMO對膠質瘤細胞的影響。建立BOC敲除小鼠皮下腫瘤模型，驗證BOC對小鼠腫瘤的作用。采用組織微陣列技術檢測正常人腦組織和膠質瘤組織中BOC和SMO的表達。在體外實驗中，boc -敲低抑制膠質瘤細胞的活力、侵襲和遷移，下調下游差異基因SMO、EGFR、HRAS和MRAS的表達。相反，smo -過表達上調了boc -敲低細胞的活力、侵襲和遷移能力。在體內，敲低boc抑制小鼠腫瘤生長，下調下游差異基因SMO、EGFR、HRAS和MRAS的表達。組織微陣列結果顯示，在膠質瘤組織中，BOC和SMO均高表達。BOC在膠質瘤患者中異常過表達并促進膠質瘤的發展。在機制上，BOC通過上調SMO、EGFR、HRAS和MRAS的表達激活Hedgehog （Hh）和RAS信號通路，從而促進膠質瘤細胞的增殖、侵襲和遷移。