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Long Non-Coding RNA TRPM2-AS Promotes Cell Migration and Invasion by Serving as a ceRNA of miR-138 and Inducing SOX4-Mediated EMT in Laryngeal Squamous Cell Carcinoma

BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is a common type of malignant tumors of larynx, and in this study, we aimed to evaluate the functional role of long non-coding RNA TRPM2-AS in LSCC. METHODS: The expression levels of TRPM2-AS in LSCC tissues and cell lines were detected by RT-qPCR...

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Detalles Bibliográficos
Autores principales: Wang, Ning, Wang, Lei, Pan, Xinliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457742/
https://www.ncbi.nlm.nih.gov/pubmed/32922080
http://dx.doi.org/10.2147/CMAR.S265412
Descripción
Sumario:BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is a common type of malignant tumors of larynx, and in this study, we aimed to evaluate the functional role of long non-coding RNA TRPM2-AS in LSCC. METHODS: The expression levels of TRPM2-AS in LSCC tissues and cell lines were detected by RT-qPCR analysis. In vitro functional assays, including MTT assay and transwell assay, were performed to explore the biological effects of TRPM2-AS on LSCC cells. The expression levels of EMT-relevant proteins were detected by Western blot analysis. The interaction between TRPM2-AS and miR-138 in LSCC, predicted by bioinformatic method, was verified by dual-luciferase reporter assay. RESULTS: We observed that TRPM2-AS was highly expressed in human LSCC tissues and cell lines. LSCC patients with advanced clinical stage exhibited higher intratumoral TRPM2-AS expression. The results of functional assays demonstrated that TRPM2-AS knockdown remarkably inhibited the proliferation, migration and invasion of LSCC cells, whereas TRPM2-AS overexpression showed opposite effects. In mechanism, we further observed that TRPM2-AS directly bound to miR-138 and served as competing endogenous RNA (ceRNA), thereby increasing SOX4 expression and promoting EMT in LSCC. The oncogenic effects of TRPM2-AS in LSCC cells were partly diminished by miR-138 restoration. CONCLUSION: In short, our findings provided first evidence that TRPM2-AS is highly expressed and exerts its oncogenic role in LSCC partly by miR-138/SOX4 axis.