Department of General Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.
Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9408-9415. doi: 10.26355/eurrev_202009_23024.
It is of significance to screen out differentially expressed long non-coding RNAs (lncRNAs) that can be utilized as tumor biomarkers in esophageal cancer. This study aims to uncover the effect of lncRNA FAM83A-AS1 on regulating migratory potential in esophageal cancer and the underlying mechanism.
Tumor tissues and adjacent normal ones were collected from 62 esophageal cancer patients for detecting FAM83A-AS1 levels. Correlations of FAM83A-AS1 with clinical indexes and overall survival of esophageal cancer patients were analyzed. Thereafter, regulatory effects of FAM83A-AS1 on migratory potential in OE19 and OE33 cells were examined by transwell and wound healing assay. Then, the target genes of FAM83A-AS1 were predicted and functionally analyzed, and a protein interaction network was constructed. Finally, the mechanism of FAM83A-AS1 in regulating the downstream gene miR-495-3p was analyzed through Luciferase assay and rescue experiments.
It was found that FAM83A-AS1 was upregulated in esophageal cancer tissues and cell lines. Higher rates of lymphatic and distant metastasis and worse survival were observed in esophageal cancer patients expressing higher level of FAM83A-AS1. Besides, the knockdown of FAM83A-AS1 suppressed migratory potential in OE19 cells, while the overexpression of FAM83A-AS1 yielded the opposite trend in OE33 cells. Moreover, miR-495-3p was indicated to be the target gene binding FAM83A-AS1, and it was lowly expressed in esophageal cancer and negatively regulated by FAM83A-AS1. Furthermore, the overexpression of miR-495-3p partially abolished the regulatory effect of FAM83A-AS1 on migratory potential in esophageal cancer.
FAM83A-AS1 is upregulated in esophageal cancer, and it stimulates migratory potential in esophageal cancer by negatively regulating miR-495-3p.
筛选出可作为食管癌肿瘤标志物的差异表达长非编码 RNA（lncRNA）具有重要意义。本研究旨在探讨 lncRNA FAM83A-AS1 对调节食管癌迁移潜能的影响及其潜在机制。
收集 62 例食管癌患者的肿瘤组织及癌旁正常组织，检测 FAM83A-AS1 水平。分析 FAM83A-AS1 与食管癌患者临床指标及总生存期的相关性。然后，通过 Transwell 和划痕愈合实验检测 FAM83A-AS1 对 OE19 和 OE33 细胞迁移潜能的调控作用。预测 FAM83A-AS1 的靶基因并进行功能分析，构建蛋白质相互作用网络。最后，通过荧光素酶报告和挽救实验分析 FAM83A-AS1 调控下游基因 miR-495-3p 的机制。
结果表明，FAM83A-AS1 在食管癌组织和细胞系中呈上调表达。FAM83A-AS1 高表达的食管癌患者淋巴结和远处转移率较高，生存状况较差。此外，FAM83A-AS1 敲低抑制了 OE19 细胞的迁移潜能，而过表达 FAM83A-AS1 则在 OE33 细胞中产生相反的趋势。此外，miR-495-3p 被确定为与 FAM83A-AS1 结合的靶基因，在食管癌中表达水平较低，受 FAM83A-AS1 负调控。此外，miR-495-3p 的过表达部分消除了 FAM83A-AS1 对食管癌迁移潜能的调节作用。
FAM83A-AS1 在食管癌中上调，通过负调控 miR-495-3p 刺激食管癌的迁移潜能。
