Lung cancer-associated transcript 1 facilitates tumorigenesis in laryngeal squamous cell carcinoma through the targeted inhibition of miR-493

Long non-coding RNAs (lncRNAs) serve important roles in the tumorigenesis of a diverse range of cancer types. The lung cancer-associated transcript 1 (LUCAT1), has been reported to promote the proliferation, migration and invasion of oral squamous cell carcinoma cells. However, the exact role of LUCAT1 in laryngeal squamous cell carcinoma (LSCC) remains to fully understood. The present study aimed to interrogate the role and modulatory mechanism of LUCAT1 in LSCC. Reverse transcription-quantitative PCR and western blotting were used to investigate the expression of LUCAT1 and miR-493, as well as the protein expression of cyclin-dependent kinase 2, cyclin E1, p21, matrix metalloproteinase (MMP)2, MMP9, vascular endothelial growth factor-C, Bcl-2, Bax, cleaved caspase-3 and procaspase-3. Cell Counting Kit-8, flow cytometry, wound healing and Transwell assays were performed to analyze the proliferation, cell cycle, apoptosis levels, and the migratory and invasive abilities, respectively, of the LSCC AMC-HN-8 cell line. In addition, dual-luciferase reporter and ribonucleoprotein immunoprecipitation assays were used to investigate the binding between LUCAT1 and microRNA (miR)-493. The results of the present study revealed that the expression levels of LUCAT1 were upregulated in AMC-HN-8 cells. The genetic knockdown of LUCAT1 expression levels significantly suppressed the cell proliferation, alongside downregulating the expression levels of CDK2 and cyclin E1 and upregulating p21 expression levels. In addition, the knockdown of LUCAT1 inhibited cell migration and invasion, as demonstrated using the wound healing and Transwell assays, respectively. Moreover, LUCAT1 knockdown promoted cell apoptosis and upregulated the expression levels of Bax and cleaved caspase-3, whilst downregulating the expression levels of Bcl-2. Furthermore, LUCAT1 was discovered to directly bind to and inhibit the well-known tumor suppressor, miR-493. Notably, the specific inhibition of miR-493 partly blocked the anticancer effects of LUCAT1 knockdown in AMC-HN-8 cells. In conclusion, these results suggested that LUCAT1 may facilitate tumorigenesis in LSCC through the targeted inhibition of miR-493, which provides evidence for a novel target for the treatment of LSCC.