ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2021
Knockdown of long non-coding RNA RP11-297P16.3 inhibits the migration and invasion of laryngeal squamous carcinoma cells.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeLaryngeal 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.
methodsSix 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.
resultsThe results show that the expression of RP11-297P16.3 in the si-lncRNA group was significantly decreased compared 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 expression of N-cadherin and vimentin was notably decreased after RP11-297P16.3 knockdown; whereas, the protein expression of cadherin was significantly increased
conclusionThese 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.
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