LncRNA UCA1 promotes cell proliferation, invasion and migration of laryngeal squamous cell carcinoma cells by activating Wnt/β‑catenin signaling pathway

Sun,Suguang; Gong,Cheng; Yuan,Kun

doi:10.3892/etm.2018.7097

LncRNA UCA1 promotes cell proliferation, invasion and migration of laryngeal squamous cell carcinoma cells by activating Wnt/β‑catenin signaling pathway

Authors:
- Suguang Sun
- Cheng Gong
- Kun Yuan
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Affiliations: Department of Otolaryngology‑Head and Neck Surgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China
Published online on: December 13, 2018 https://doi.org/10.3892/etm.2018.7097
Pages: 1182-1189
Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

In view of the poor prognosis of laryngeal squamous cell carcinoma (LSCC) and the functionality of long non‑coding (lnc)RNA UCA1 in different types of cancer, the present study aimed to investigate the role of UCA1 in the development and progression of LSCC. A total of 90 patients with LSCC and 90 healthy subjects were enrolled in the present study. Expression levels of UCA1 in tumor tissues and adjacent healthy tissues, as well as serum of patients with LSCC and normal controls were detected by reverse transcription‑quantitative polymerase chain reaction. Receiver operating characteristic curve analysis was performed to evaluate the diagnostic value of serum UCA1 for LSCC. Survival curves were plotted using the Kaplan‑Meier method and employed to evaluate the prognosic values of serum UCA1 for LSCC. Cell proliferation, migration and invasion were detected using the cell proliferation assay, and Transwell migration and invasion assays, respectively. Expression levels of Wnt/β‑catenin‑associated proteins were detected by western blot analysis. Results indicated that the expression levels of UCA1 were significantly higher in tumor tissues compared with adjacent healthy tissues in the majority of patients with LSCC. In addition, serum levels of UCA1 were significantly higher in patients with LSCC coapred with healthy controls. UCA1 overexpression promoted, whereas UCA1 knockdown inhibited the proliferation, migration and invasion of LSCC cells. UCA1 overexpression activated the Wnt/β‑catenin signaling pathway in LSCC cells, whereas treatment with Wnt inhibitor reduced the enhancing effects of UCA1 overexpression on the proliferation, migration and invasion of LSCC cells. The present findings suggest that UCA1 can promote cell proliferation, invasion and migration of LSCC cells by activating the Wnt/β‑catenin signaling pathway.

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