摘要
通过将假基因RPL34-PS1的序列克隆至MSCV-PIG载体上后,包装反转录病毒并感染小鼠B淋巴瘤细胞38B9,构建稳定过表达RPL34-PS1的38B9细胞系。对体外培养的细胞进行计数观察细胞增殖;利用流式检测技术观察细胞的凋亡和周期;进行小鼠皮下荷瘤试验观察体内成瘤并进行相关机制研究。结果表明:假基因RPL34-PS1对体外培养的38B9的生长速率、周期及凋亡无显著影响,但在体内能显著增加B细胞淋巴瘤的生长,其促进体内肿瘤生长的机制可能是肿瘤微环境中T淋巴细胞数量的减少之故,说明RPL34-PS1在微环境中靶向免疫细胞以促进肿瘤生长,RPL34-PS1可能可作为B细胞淋巴瘤的临床治疗的一个潜在靶点。
Pseudogene RPL34-PS1 was cloned into RNA-expressing retroviral vector MSCV-PIG;mouse B lymphoma 38 B9 cells were infected with RPL34-PS1 retrovirus;cells were counted in culture;apoptosis and cell cycle were measured using flow cytometer;tumor-bearing experiments were performed to observe tumor growth in vivo. Results showed that RPL34-PS1 had no significant effect on the growth, cell cycle and apoptosis of 38 B9 cultured in vitro. However, RPL34-PS1 significantly promoted the growth of 38 B9 lymphoma cells in vivo. The underlying mechanism of tumor growth in vivo might be due, at least in part, to the decrease in the number of T-lymphocytes in the tumors. These results indicate that RPL34-PS1 can target immune cells in microenvironment to sustain tumor growth, and thus RPL34-PS1 might be a potential therapeutic target for B-cell lymphomas.
作者
刘金晶
周芳超
张毅
郁多男
LIU Jinjing;ZHOU Fangchao;ZHANG Yi;YU Duonan(Jiangsu Key Laboratory of Experimental&Translational Non-Coding RNA Research/College of Medicine,Yangzhou University,Yangzhou 225009,China)
出处
《扬州大学学报(农业与生命科学版)》
CAS
北大核心
2021年第2期52-56,67,共6页
Journal of Yangzhou University:Agricultural and Life Science Edition
基金
国家自然科学基金面上项目(81670186、81870096)。