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H3K27ac-induced FOXC2-AS1 accelerates tongue squamous cell carcinoma by upregulating E2F3
Cuiting Chen1, Qiongyu Chen1, Jian Wu1
1Department of Stomatology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Background:
The important roles of lncRNAs have been reported in cancers, including tongue squamous cell carcinoma (TSCC). Here, we investigated the functional role and molecular mechanisms of lncRNA FOXC2-AS1 in TSCC.
Methods:
The expression level of FOXC2-AS1 in TSCC was determined by RT-qPCR. Its biological role was evaluated through colony formation assay, flow cytometry, wound healing, transwell, and Western blot analyses. The interactions among gene were tested by mechanistic investigations.
Results:
FOXC2-AS1 expression was high in TSCC tissues and cells. Functional assays in vitro showed that silencing FOXC2-AS1 restrained cell proliferation, cell cycle, migration, invasion, and EMT. In the mechanism, it was verified that H3K27 acetylation (H3K27ac) triggered an increase in FOXC2-AS1 expression. Furthermore, FOXC2-AS1 was identified as a cytoplasmic lncRNA and served as a ceRNA to upregulate E2F3 expression via sponging miR-6868-5p.
Conclusion:
H3K27ac-induced FOXC2-AS1 exhibits carcinogenic property in TSCC by the miR-6868-5p/E2F3 axis.
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