Long non‑coding RNA MIAT promotes the proliferation and invasion of laryngeal squamous cell carcinoma cells by sponging microRNA‑613
- Fucun Song
- Yang Yang
- Jixiang Liu
Affiliations: Department of Otolaryngology Head and Neck Surgery, Tianjin Union Medical Center, Tianjin 300121, P.R. China
- Published online on: January 21, 2021 https://doi.org/10.3892/etm.2021.9663
Copyright: © Song
et al. This is an open access article distributed under the
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Accumulating evidence indicates that the long non‑coding RNA myocardial infarction associated transcript (lncRNA MIAT) serves an important role in the progression of a number of cancer types. However, the precise molecular mechanism of MIAT in laryngeal squamous cell carcinoma (LSCC) progression remain elusive. The aim of the current study was to assess the effects and to clarify the molecular mechanism of MIAT on the proliferation and invasion of LSCC cells. The expression of MIAT was detected in LSCC tissues and cells using reverse transcription‑quantitative PCR. MTT and colony formation assays were performed to examine the effects of MIAT on the proliferation of LSCC cells. Additionally, wound healing and Transwell experiments were employed to examine cellular migration and invasion. Luciferase reporter gene assay was also used to confirm the direct binding between MIAT and microRNA (miR)‑613 in LSCC cells. An RNA immunoprecipitation assay was performed to verify the interaction between MIAT and miR‑613. In the present study, it was found that the expression of MIAT in LSCC tissues was markedly higher compared with that in adjacent non‑tumor tissues. In addition, MIAT expression was also increased in the human LSCC cell lines TU686, TU‑177 and AMC‑HN‑8 compared with that in normal human keratinocytes (HaCaT). Knocking down MIAT expression significantly reduced LSCC cell proliferation and inhibited colony formation, a shown by MTT and colony formation assays, respectively. MIAT knockdown also substantially inhibited the migratory and invasive abilities of LSCC cells, as shown by wound healing and Transwell invasion assays, respectively. Subsequently, luciferase reporter assays verified that MIAT could bind to miR‑613, where a negative correlation was observed between the expression of MIAT and miR‑613 in LSCC tissues. Suppression of miR‑613 partially reversed the inhibitory effects of MIAT knockdown on the proliferation, migration and invasion of LSCC cells. Taken together, the present study identified that MIAT may function as an oncogenic lncRNA to promote LSCC progression, which provides a potential therapeutic target or as a novel diagnostic biomarker for LSCC.