Abstract
Although long non-coding RNAs (lncRNAs) have been implicated in various human cancer types, the role of lncRNA ezrin antisense RNA 1 (EZR-AS1) in cutaneous squamous cell carcinoma (cSCC) remains unclear. The present study aimed to investigate the effect of lncRNAEZR-AS1 on cSCC and identify the underlying molecular mechanisms. EZR-AS1 expression was measured in cSCC tissue and cells detected using reverse transcription-quantitative PCR. Gain-of-function assays were performed in A431 cells, which have a relatively low expression of EZR-AS1, while loss-of-function assays were performed in SCC13 and SCL-1 colon cancer cells, which have a relatively high expression of EZR-AS1. Cell viability, proliferation, migration, invasion and apoptosis were assessed using MTT, plate cloning, wound healing, Transwell and flow cytometry assays, respectively. EZR-AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively. Compared with the small interfering RNA (si)-negative control (NC) group, si-EZR-AS1 significantly inhibited SCC13 and SCL-1 cell proliferation, migration and invasion, but promoted cell apoptosis. By contrast, compared with the pc-NC group, EZR-AS1 overexpression significantly enhanced A431 cell proliferation, migration and invasion, but inhibited cell apoptosis. Moreover, focal adhesion kinase (FAK) was identified as a target of EZR-AS1, and EZR-AS1 knockdown significantly decreased FAK expression compared with the si-NC group. Moreover, EZR-AS1 knockdown significantly downregulated the protein expression levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT in cSCC cells compared with the si-NC group. The PI3K agonist 740Y-P significantly reversed si-EZR-AS1-mediated effects on SCC13 and SCL-1 cell proliferation, migration, invasion and apoptosis. In conclusion, the present study demonstrated that si-EZR-AS1 inhibited cSCC cell proliferation, migration and invasion, and promoted cell apoptosis, potentially via regulating the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC.
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