LncRNA FEZF1-AS1 accelerates the migration and invasion of laryngeal squamous cell carcinoma cells through miR-4497 targeting GBX2.

Autor: Chen X; Department of Otolaryngology, First Hospital of Ningbo City, Ningbo, Zhejiang, 315000, People's Republic of China. chenxudong_xdc@163.com., Cheng P; Department of Otolaryngology, First Hospital of Ningbo City, Ningbo, Zhejiang, 315000, People's Republic of China., Hu C; Department of Otolaryngology, First Hospital of Ningbo City, Ningbo, Zhejiang, 315000, People's Republic of China.
Jazyk: angličtina
Zdroj: European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery [Eur Arch Otorhinolaryngol] 2021 May; Vol. 278 (5), pp. 1523-1535. Date of Electronic Publication: 2021 Feb 07.
DOI: 10.1007/s00405-021-06636-5
Abstrakt: Background: MiR-4497 has been previously proved to exert an anti-cancer role in laryngeal squamous cell carcinoma (LSCC) by negatively regulating gastrulation brain homeobox 2 (GBX2). However, the mechanism of miR-4497 in LSCC has yet to be fully elucidated. This study intended to investigate the role of FEZF1-AS1 in the migration and invasion of LSCC cells and clarified its mechanism through miR-4497 and GBX2.
Methods: qPCR evaluated the expression of FEZF1-AS1, miR-4497 and GBX2 in LSCC tissues and cells, compared with controls. Western blotting analyzed GBX2, E-cadherin, N-cadherin and Vimentin. CCK8, wound healing and transwell assays assessed the viability, migration and invasion of TU686 and UM-SCC-17A cells. Luciferase reporter assay affirmed the interplay of miR-4497 with FEZF1-AS1 or GBX2 and Pearson's correlation analysis explored the association between each two genes in both tumor and non-tumor tissues.
Results: FEZF1-AS1 was highly expressed in LSCC tissues and cells. Silence or elevation of FEZF1-AS1 inhibited or promoted the migration and invasion of TU686 and UM-SCC-17A cells. FEZF1-AS1 targeted and negatively modulated miR-4497. Inhibition of miR-4497 markedly restored the FEZF1-AS1 silence-repressed cell viability of TU686 and UM-SCC-17A cells. Further, FEZF1-AS1 could positively regulate GBX2 via negative regulation of miR-4497. In these two cells, GBX2 deficiency reversed the promoting impacts of miR-4497 repression on migration and invasion.
Conclusion: Taken together, FEZF1-AS1, heightened in LSCC tissues and cells, promotes cell migration and invasion of LSCC cells via targeting miR-4497 that inhibits GBX2. The finding may offer new options for the treatment of this cancer.
Databáze: MEDLINE
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