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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.

ABSTRACT: 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‑β (TGF‑β) 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‑β‑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.

SUBMITTER: Cui W

PROVIDER: S-EPMC6521927 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Laryngeal squamous cell carcinoma (LSCC) is a highly invasive malignant tumor in the head and neck area. As an oncogene, long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion several types of cancer. The present study aimed to reveal the effects of NEAT1 on the progression of LSCC. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect relative mRNA expression levels of NEAT1, microRNA (miR)-204-5p and semaphorin (SEMA) 4B. Kaplan-Meier analysis was used to analyze overall survival times. RNA in-situ hybridization (ISH) exhibited the distribution of NEAT1 and miR-204-5p in tissues. RNA fluorescence ISH was used to analyze the distribution of NEAT1 and miR-204-5p in the cells. Western blot analysis was used to detect the expression level of target proteins. Cell viability was analyzed using a MTT assay, while flow cytometry was used to determine cell apoptosis. Wound healing and Transwell invasion assays were used to value cell migration and invasion, respectively. RNA immunoprecipitation assay, bioinformatics prediction and a dual luciferase reporter assay were used to analyze the target relationship. The RT-qPCR results showed that NEAT1 was highly expressed and miR-204-5p had decreased expression in LSCC tissues and cells compared with that in the normal tissue and the 16HBE-14o cell line, respectively. Knockdown of NEAT1 using small interfering (si) RNA and overexpressed miR-204-5p both effectively inhibited the proliferation, migration and invasion of LSCC cells. Besides, further experiments revealed that miR-204-5p was a target of NEAT1. At the same time, silenced miR-204-5p reversed the anti-tumor effects of si-NEAT1. In addition, SEMA4B was targeted by miR-204-5p in LSCC cells and upregulated SEMA4B weakened the antitumor effects of miR-204-5p in LSCC cells. NEAT1 regulated the expression of SEMA4B by targeting miR-204-5p in LSCC cells. Overall, NEAT1 promoted the proliferation and invasion of LSCC cells by regulating the miR-204-5p/SEMA4B axis.

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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.

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