Silencing the lncRNA NORAD inhibits EMT of head and neck squamous cell carcinoma stem cells via miR‑26a‑5p.

Cancer stem cells are closely associated with tumor metastasis or recurrence. According to previous literature reports, microRNA (miR)‑26a has an inhibitory effect on head and neck squamous cell carcinoma (HNSCC), and the long non‑coding RNA (lncRNA) non‑coding RNA activated by DNA damage (NORAD) has been found to interact with miR‑26a‑5p. The present study aimed to investigate the regulation and mechanism of NORAD and miR‑26a‑5p in the epithelial‑mesenchymal transition (EMT) of HNSCC stem cells. An ALDEFLUOR stem cell detection kit, a flow cytometer, a self‑renewal ability test and western blotting were used to sort and identify HNSCC stem cells. The ENCORI website and a dual‑luciferase assay were used to assess the relationship between genes. The mRNA and protein expression levels of NORAD, miR‑26a‑5p and EMT‑related genes were detected via reverse transcription‑quantitative PCR and western blotting. Functional experiments (MTT assay, flow cytometry, wound healing assay and Transwell assay) were conducted to analyze the effects of NORAD and miR‑26a‑5p on HNSCC stem cells. The successfully sorted aldehyde dehydrogenase (ALDH) cells had a self‑renewal capacity and displayed upregulated expression levels of CD44, Oct‑4 and Nanog. NORAD knockdown, achieved using small interfering (si)RNA, downregulated the expression levels of tumor markers in ALDH cells. siNORAD inhibited cell vitality, migration and invasion, as well as promoted apoptosis, increased the expression of epithelial cell markers and decreased the expression of interstitial cell markers in HNSCC stem cells. miR‑26a‑5p was a downstream gene of NORAD, and knockdown of miR‑26a‑5p partially offset the regulatory effect of siNORAD on HNSCC stem cells. Collectively, the present study demonstrated that NORAD knockdown attenuated the migration, invasion and EMT of HNSCC stem cells via miR‑26a‑5p.