Knockdown of long non‑coding RNA RP11‑297P16.3 inhibits the migration and invasion of laryngeal squamous carcinoma cells
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[1] Shanxi Medical University
Shanxi Medical University
China
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- Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 23, Nº. 10, 2021, págs. 2057-2065
- Idioma: inglés
- Enlaces
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Resumen
Purpose Laryngeal cancer has a poor prognosis when progressing to an advanced stage with limited treatment options.
Therefore, understanding the underlying mechanisms is important to identify novel treatment targets. Long non-coding RNAs (lncRNAs) have been shown to play oncogenic roles in cancer, including in laryngeal cancer. We previously discovered that the lncRNA RP11-297P16.3 is overexpressed in laryngeal squamous cell carcinoma (LSCC) based on RNA-sequencing data.
Therefore, the aim of the present study was to investigate the effects of knockdown of RP11-297P16.3 on the migration and invasion of LSCC cells, and the significance of these effects.
Methods Six methods were employed to assess the function of RP11-297P16.3 including gene silencing, RT-PCR, the 5-Ethynyl-20-deoxyuridine (EdU) staining assay, Scratch wound-healing assay, transwell assay, and Western blot.
Results The results show that the expression of RP11-297P16.3 in the si-lncRNA group was significantly decreased com- pared with those in the BC (blank control) and NC (negative control) groups. Moreover, knockdown of RP11-297P16.3 significantly inhibited the migration and invasion of LSCC cells but had no effect on cell proliferation. The protein expres- sion of N-cadherin and vimentin was notably decreased after RP11-297P16.3 knockdown; whereas, the protein expression of cadherin was significantly increased Conclusion These results suggested that RP11-297P16.3 may inhibit the migration and invasion of LSCC cells by regulating the epithelial–mesenchymal transition process, suggesting that RP11-297P16.3 is a potential new target for treating LSCC
