Page 39 - 南京医科大学自然版

第45卷第6期 南京医科大学学报（自然科学版）
2025年6月 Journal of Nanjing Medical University（Natural Sciences） ·777 ·

·基础研究·

Akt1上调FBXO6表达对胶质瘤细胞增殖和侵袭的影响

高彩月 ，曹丹丹 ，倪思琦 ，张 婧 ，王迎伟 ，邱 文 ，赵晨卉 3*
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南京医科大学基础医学院免疫学系，第一临床医学院临床医学系（长学制），江苏 南京 211166；南京医科大学第一附属医
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院肿瘤科，江苏 南京 210029
［摘 要］ 目的：检测胶质瘤组织和细胞中F 盒蛋白（F⁃box protein，FBXO）6的表达及其对胶质瘤细胞增殖和侵袭的影响，并
探究FBXO6表达的上游调控机制。方法：使用CGGA数据库分析胶质瘤患者肿瘤组织中FBXO6的表达及其与患者预后的相
关性。行RT⁃PCR 和Western blot 检查胶质瘤细胞系（U251、U373和U87）中FBXO6的表达水平，筛选出FBXO6蛋白表达量最
高的U87细胞。CCK⁃8和Transwell 实验检测过表达和沉默FBXO6对U87细胞增殖和侵袭的影响。使用U0126（ERK1/2抑制
剂）、SP600125（JNK抑制剂）和Perifosine（Akt1抑制剂）处理U87细胞，Western blot 检查ERK1/2、JNK、Akt1的表达和磷酸化水
平，之后行RT⁃PCR和Western blot检测FBXO6的表达变化，CCK⁃8和Transwell实验检测U87细胞增殖和侵袭能力。使U87细
胞过表达FBXO6并给予Perifosine 处理，进行RT⁃PCR、Western blot、CCK⁃8和Transwell 实验，检测FBXO6表达、细胞增殖和侵
袭能力。结果：胶质瘤患者癌组织中FBXO6高表达，且表达量与恶性程度相关，并与患者不良预后密切相关。3种胶质瘤细胞
系U251、U373和U87均表达FBXO6，以U87细胞表达最为显著。过表达FBXO6基因后U87细胞的增殖和侵袭明显增强，而沉
默FBXO6基因后U87细胞的增殖和侵袭明显减弱。Akt1抑制剂可显著下调U87细胞的FBXO6表达，而ERK1/2和JNK抑制剂
对FBXO6的表达无明显影响。Akt1抑制剂可显著减弱U87细胞的增殖和侵袭，而过表达FBXO6可拮抗上述效应。结论：胶质
瘤细胞中Akt1活化上调FBXO6基因的表达，促进细胞的增殖和侵袭。
［关键词］ 胶质瘤；FBXO6；Akt1；增殖；侵袭
［中图分类号］ R739.41 ［文献标志码］ A ［文章编号］ 1007⁃4368（2025）06⁃777⁃09
doi：10.7655/NYDXBNSN241268

The effects of Akt1 upregulated FBXO6 expression on the proliferation and invasive of
glioma cells
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GAO Caiyue ，CAO Dandan ，NI Siqi ，ZHANG Jing ，WANG Yingwei ，QIU Wen ，ZHAO Chenhui 3*
Department of Immunology，School of Basic Medicine，Department of Clinical Medicine，the First Clinical Medical
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College，Nanjing Medical University，Nanjing 211166；Department of Oncology，the First Affiliated Hospital of
Nanjing Medical University，Nanjing 210029，China
［Abstract］ Objective：To examine the expression of F ⁃ box protein（FBXO）6 in glioma tissues and cells and its impact on the
proliferation and invasion of glioma cells，and to explore the upstream regulatory mechanism of FBXO6 expression. Methods：The
CGGA database was used to analyze the expression of FBXO6 in tumor tissues of glioma patients and its correlation with patient
prognosis. RT⁃PCR and Western blot were performed to check the expression levels of FBXO6 in glioma cell lines（U251，U373，and
U87），and U87 cells with the highest expression were screened out. RT⁃PCR，Western blot，CCK⁃8，and Transwell experiments were
carried out to detect the effects of FBXO6 overexpression and silencing on the proliferation and invasion of U87 cells. U87 cells were
treated with U0126（an ERK1/2 inhibitor），SP600125（a JNK inhibitor），and Perifosine（an Akt1 inhibitor），and Western blot was
conducted to examine the expression and phosphorylation levels of ERK1/2，JNK and Akt1. Subsequently，RT⁃PCR and Western blot
were used to detect the expression changes of FBXO6，and then CCK⁃8 and Transwell experiments were performed to measure the
proliferation and invasion capabilities of U87 cells. FBXO6 was overexpressed in U87 cells，which were then treated with Perifosine，
and RT⁃PCR，Western blot，CCK⁃8，and Transwell experiments were carried out to investigate the levels of FBXO6 expression，cell

［基金项目］ 国家自然科学基金（81902878）；江苏省高等学校大学生创新训练计划项目（202010312039Y）
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通 信 作 者（Corresponding author），E⁃mail：qiuwen@njmu.edu.cn（ORCID：0000⁃0003⁃2097⁃9773）；chenhuizhao@njmu.edu.cn
（ORCID：0000⁃0002⁃7950⁃5225）