Gai Qimei, Guo Wei, Liu Junlian
Department of Vascular Surgery, The Affiliated Yantai Yuhuangding HospitaI of Qingdao University Medical College, Yantai, China.
J BUON. 2021 Mar-Apr;26(2):380-387.
In the early stage, bioinformatics analysis revealed that the expression of long-chain non-coding RNA LINC00963 in glioma tissues was remarkably increased, but its biological effects on glioma and the potential molecular mechanisms have not been reported. This study aimed to conduct a preliminary discussion on the impact of LINC00963 on glioma, so as to provide new ideas for the treatment of this cancer.
GEPIA database was consulted to determine the expression level of LINC00963 in gliomas. In addition, the interplay between LINC00963 expression and the prognosis of glioma patients was analyzed by Kaplan-Meier method. Effects of LINC00963 on the proliferation and migration of glioma cells were determined using Cell Counting Kit (CCK-8) and Transwell assay. The subcellular localization of LINC00963 was determined by nuclear separation experiments. At the same time, the regulation of LINC00963 on p21 expression was verified through qRT-PCR and Western blot experiments.
By analyzing the GEPIA database, we found that LINC00963 was highly expressed in glioma tissues. Meanwhile, qRT-PCR results revealed that LINC00963 level in glioma tissues and cell lines was remarkably higher than that in the normal control group. Kaplan-Meier and log-rank test revealed that there was no statistically significant association between the expression level of LINC00963 and the prognosis of patients with glioma. In addition, in vitro cell assay results indicated that downregulation of LINC00963 markedly suppressed the proliferation and invasiveness of glioma cells. Finally, the related mechanism analysis revealed that LINC00963 may inhibit p21 expression through modulation of EZH2.
LINC00963 can inhibit p21 expression through EZH2 and thus enhance the proliferative and invasive capacities of glioma cells. Consequently, LINC00963 may be a potential therapeutic target for gliomas.
早期的生物信息学分析显示，长链非编码RNA LINC00963在胶质瘤组织中的表达显著增加，但其对胶质瘤的生物学作用及潜在分子机制尚未见报道。本研究旨在对LINC00963对胶质瘤的影响进行初步探讨，为该癌症的治疗提供新思路。
查阅GEPIA数据库以确定LINC00963在胶质瘤中的表达水平。此外，采用Kaplan-Meier法分析LINC00963表达与胶质瘤患者预后之间的相互关系。使用细胞计数试剂盒（CCK-8）和Transwell实验检测LINC00963对胶质瘤细胞增殖和迁移的影响。通过细胞核分离实验确定LINC00963的亚细胞定位。同时，通过qRT-PCR和蛋白质免疫印迹实验验证LINC00963对p21表达的调控作用。
通过分析GEPIA数据库，我们发现LINC00963在胶质瘤组织中高表达。同时，qRT-PCR结果显示，胶质瘤组织和细胞系中LINC00963水平显著高于正常对照组。Kaplan-Meier分析和对数秩检验显示，LINC00963表达水平与胶质瘤患者预后之间无统计学意义上的关联。此外，体外细胞实验结果表明，下调LINC00963可显著抑制胶质瘤细胞的增殖和侵袭能力。最后，相关机制分析显示，LINC00963可能通过调节EZH2抑制p21表达。
LINC00963可通过EZH2抑制p21表达，从而增强胶质瘤细胞的增殖和侵袭能力。因此，LINC00963可能是胶质瘤的一个潜在治疗靶点。
