lncRNA TUG1 promotes the development of oral squamous cell carcinoma by regulating the MAPK signaling pathway by sponging miR-593-3p

基因敲除 MAPK/ERK通路 基因沉默 生物 癌症研究 小RNA 细胞生长 细胞凋亡 基底细胞 细胞生物学 细胞 信号转导 基因 医学 遗传学 病理
作者
Lei Jiang,Bing Zhou,Dongjie Fu,Bo Cheng
出处
期刊:Cell Cycle [Informa]
卷期号:21 (17): 1856-1866 被引量:2
标识
DOI:10.1080/15384101.2022.2074624
摘要

Dysregulation of non-coding RNAs (ncRNAs) has been proved to play important roles in oral squamous cell carcinoma (OSCC). This study aimed to determine the combined role of lncRNA TUG1, miR-593-3p, and MAPK signaling in oral squamous cell carcinoma (OSCC) development. Here, we found that TUG1 was up-regulated in OSCC tissues and cell lines. Silencing TUG1 suppressed proliferation migration, invasion and promoted apoptosis of OSCC cells. We also validated that knockdown of TUG1 suppressed MAPK signaling pathway and inhibited EMT process in OSCC cells. Then, a novel LncRNA TUG1/ miR-593-3p/MAPK axis was verified to rescue cell viability in OSCC cells. Mechanistically, miR-593-3p bound to lncRNA TUG1, and lncRNA TUG1 positively regulated MAPK related proteins through acting as RNA sponger for miR-593-3p. Further gain- and loss-of-function experiments evidenced that the protective effects of lncRNA TUG1 knock-down on OSCC cells were abrogated by silencing miRNA-593-3p. The OSCC nude mice model experiments demonstrated that depletion of TUG1 further inhibited tumor growth. In conclusion, appropriate diagnostic biomarkers and therapies for OSCC can be identified by targeting the TUG1/miR-593-3p/MAPK axis.

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