The positive feedback loop between ILF3 and lncRNA ILF3-AS1 promotes melanoma proliferation, migration, and invasion

作者：Guozhen Gao, Wenjun Li, Sha Liu, Dongmei Han, Xingwei Yao, Juanjuan Jin, Dezhi Han, Weijing Sun, Xiangjun Chen · 发表于：Cancer Management and Research · 年份：2018 · DOI：10.2147/cmar.s186777 · 被引用次数：19 · 研究领域：Cancer-related molecular mechanisms research、RNA regulation and disease、MicroRNA in disease regulation

Purpose: In our previous study, we identified that lncRNA ILF3 antisense RNA 1 (ILF3-AS1) is increased and has oncogenic roles in melanoma. However, the cause of the upregulation of ILF3-AS1 and the modulation between ILF3-AS1 and ILF3 in melanoma are still unknown. This study aimed to investigate the significances of the interaction between ILF3-AS1 and ILF3 in melanoma. Materials and methods: The expression of ILF3 in melanoma tissues and cell lines was measured by quantitative real-time PCR (qRT-PCR). The interactions between ILF3-AS1 and ILF3 were explored by the RNA immunoprecipitation assay, the transcription inhibition assay, qRT-PCR, the chromatin immunoprecipitation assay, and Western blot. Gain-of-function and loss-of-function assays were performed to investigate the effects of ILF3 and ILF3-AS1 on melanoma proliferation, migration, and invasion. Results: ILF3 is also increased in melanoma tissues and cell lines. Increased expression of ILF3 predicts poor survival of melanoma patients. Mechanistic investigation revealed that ILF3 directly binds ILF3-AS1, increases ILF3-AS1 transcript stability, and upregulates ILF3-AS1 transcript levels. ILF3-AS1 represses the binding of EZH2 to the promoter of ILF3 , induces euchromatin formation at ILF3 promoter, and activates ILF3 transcription. Thus, ILF3 and ILF3-AS1 form positive feedback loop, which induces the upregulation of ILF3 and ILF3-AS1 in melanoma. The expression of ILF3-AS1 is positively correlated with ILF3 in mela...