Hou Anli, Zhang Yali, Fan Yujuan, Zheng Yi, Zhou Xiuying, Liu Huilan
Department of Gynaecology, University of Chinese Academy of Sciences Shenzhen Hospital, Shenzhen City, Guangdong Province 518106, People's Republic of China.
Department of Gynaecology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 067000, People's Republic of China.
Cancer Manag Res. 2020 Jun 3;12:4209-4216. doi: 10.2147/CMAR.S224067. eCollection 2020.
The incidence of cervical squamous cell carcinoma (CSCC) has expanded in recent years. However, the function of long non-coding RNA (lncRNA) MAGI2-AS3 in the occurrence and progression of CSCC remains unclear. Therefore, the role of lncRNA MAGI2-AS3 in cervical squamous cell carcinoma (CSCC) was investigated in our study.
We used qRT-PCR analysis to identify the level of MAGI2-AS3 mRNA expression in CSCC clinical samples and cell lines. We investigated cell migration and invasion of CSCC cells transfected with MAGI2-AS3, miR-233 mimic, or EPB41L3 with transwell assays. Bioinformatics analysis and a luciferase reporter assay were employed to predict the interaction between MAGI2-AS3 and miR-233.
We found that MAGI2-AS3 and EPB41L3 were both downregulated in CSCC and the expression of this two was positively correlated. Bioinformatics analysis showed that MAGI2-AS3 might bind to miR-233, which could directly target EPB41L3. In CSCC cells, overexpression of MAGI2-AS3 led to upregulated, while overexpression of miRNA-233 led to downregulated expression of EPB41L3. However, MAGI2-AS3 and miR-233 did not affect the expression of each other. In addition, overexpression of MAGI2-AS3 and EPB41L3 led to inhibited cancer cell invasion and migration, while overexpression of miR-233 played an opposite role and attenuated the effects of overexpressing MAGI2-AS3.
MAGI2-AS3 may sponge miR-233 to upregulate EPB41L3, thereby inhibiting CSCC cell invasion and migration.
近年来，宫颈鳞状细胞癌（CSCC）的发病率有所上升。然而，长链非编码RNA（lncRNA）MAGI2-AS3在CSCC发生发展中的作用仍不清楚。因此，本研究探讨lncRNA MAGI2-AS3在宫颈鳞状细胞癌（CSCC）中的作用。
我们采用qRT-PCR分析来确定CSCC临床样本和细胞系中MAGI2-AS3 mRNA的表达水平。我们通过Transwell实验研究了转染MAGI2-AS3、miR-233模拟物或EPB41L3的CSCC细胞的迁移和侵袭能力。采用生物信息学分析和荧光素酶报告基因实验来预测MAGI2-AS3与miR-233之间的相互作用。
我们发现MAGI2-AS3和EPB41L3在CSCC中均下调，且二者表达呈正相关。生物信息学分析表明，MAGI2-AS3可能与miR-233结合，而miR-233可直接靶向EPB41L3。在CSCC细胞中，MAGI2-AS3的过表达导致EPB41L3表达上调，而miRNA-233的过表达导致EPB41L3表达下调。然而，MAGI2-AS3和miR-233彼此不影响对方的表达。此外，MAGI2-AS3和EPB41L3的过表达导致癌细胞侵袭和迁移受到抑制，而miR-233的过表达则起到相反作用，并减弱了MAGI2-AS3过表达的影响。
MAGI2-AS3可能通过吸附miR-233上调EPB41L3，从而抑制CSCC细胞的侵袭和迁移。
