TGF-β-induced long non-coding RNA MIR155HG promotes the progression and EMT of laryngeal squamous cell carcinoma by regulating the miR-155-5p/SOX10 axis

Non-coding RNAs, particularly long non-coding RNAs (lncRNAs), play important roles in tumorigenesis. The miR-155 host gene (MIR155HG) lncRNA has been found to play a crucial role in tumor progression. However, the role of MIR155HG in laryngeal squamous cell carcinoma (LSCC) remains unclear. Thus, the aim of the present study was to explore the roles and underlying molecular mechanisms of action of MIR155HG and miR-155-5p in LSCC, in an effort to provide novel approaches for the antitumor therapy for LSCC. In the present study, the expression levels of miR-155-5p and MIR155HG were detected by reverse tran scription-quantitative polymerase chain reaction. In addition, the biological functions of MIR155HG and miR-155-5p on LSCC were evaluated in vitro by MTS assay, colony formation assay and Transwell assays, and in vivo by tumorigenesis assays. It was revealed that MIR155HG and miR-155-5p were significantly upregulated in LSCC tissues, and were associated with the TNM stage, pathological differentiation and lymph node metastasis. Moreover, the knockdown of MIR155HG and miR-155-5p inhibited the proliferation, migration and invasion of LSCC cells, whereas their overexpression exerted the opposite effects in vitro and MIR155HG overexpression promoted tumorigenesis in vivo. Furthermore, MIR155HG downregulation reduced the expression level of miR-155-5p. The inhibitory effect of MIR155HG knockdown on malignant behavior was abrogated by miR-155-5p overexpression. Bioinformatics analysis and luciferase reporter assay confirmed that miR-155-5p contributed to the progression of LSCC by directly binding to the 3 ' untranslated region of SRY-related-HMG-box 10 (SOX10). In addition, MIR155HG and miR-155-5p were upregulated by the induction of transforming growth factor-beta (TGF-beta) and promoted the expression of mesenchymal markers synergistically. On the whole, the findings of the present study indicate a novel role of MIR155HG in the TGF-beta-induced EMT of LSCC cells by regulating EMT markers through the miR-155/SOX10 axis. The MIR155HG/miR-155-5p/SOX10 axis plays an important role in promoting the progression of LSCC and may thus serve as a potential therapeutic target for LSCC treatment.