lncRNA SOX2‑OT regulates laryngeal cancer cell proliferation, migration and invasion and induces apoptosis by suppressing miR‑654
- Guang Li
- Chunchen Pan
- Jiaqiang Sun
- Guanglun Wan
- Jingwu Sun
Affiliations: School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China, Department of Otorhinolaryngology‑Head and Neck Surgery, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, P.R. China
- Published online on: March 6, 2020 https://doi.org/10.3892/etm.2020.8577
Copyright: © Li
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Laryngeal carcinoma is the most common type of malignant tumor in the head and neck. Long non‑coding RNAs (lncRNAs) serve crucial roles in numerous biological processes. The present study aimed to investigate the role of lncRNA SOX2‑OT in laryngeal cancer and to reveal the underlying mechanisms. Reverse transcription‑quantitative PCR assays were used to measure the expression levels of SOX2‑OT in the laryngeal cell lines. Furthermore, cell proliferation, apoptosis, migration and invasion were assessed by CCK‑8, flow cytometry, wound healing and Transwell assays, respectively. Western blot assay was performed to detect the protein expressions. In addition, a dual‑luciferase reporter assay was performed to confirm the direct interaction between SOX2‑OT and microRNA (miR)‑654. The data demonstrated that SOX2‑OT level were significantly increased in the laryngeal cell lines. Furthermore, SOX2‑OT silencing markedly promoted apoptosis and suppressed the proliferation, migration and invasion of TU‑177 cells. A dual‑luciferase reporter assay revealed that miR‑654 was a direct target of SOX2‑OT. Moreover, downregulation of miR‑654 could attenuate cell apoptosis and accelerate cell proliferation, migration and invasion in TU‑177 cells. In summary, the present study reported that knockdown of SOX2‑OT could suppress cell proliferation, migration and invasion, and induce apoptosis in laryngeal cancer by targeting miR‑654.