Abstract
Long non-coding RNA (lncRNA) has been verified to participate in the tumour regulation, including oral squamous cell carcinoma (OSCC). Nevertheless, the role of lncRNA SNHG20 on OSCC still remains elusive. Here, we investigate the physiopathologic functions of lncRNA SNHG20 in OSCC tumorigenesis and explore its potential mechanism. LncRNA SNHG20 was up-regulated in OSCC tissue compared with adjacent non-tumour tissue. Meanwhile, SNHG20 was overexpressed in cancer stem-like cells. In vitro and in vivo, loss-of-function experiments showed that lncRNA SNHG20 knockdown inhibited proliferative ability, mammosphere-forming ability, ALDH1 expression, stem factors (LIN28, Nanog, Oct4, SOX2) and tumour growth. Bioinformatics and luciferase reporter assay revealed that miR-197 targeted the 3'-untranslated regions of SNHG20 and LIN28 by complementary binding. Validation experiments confirmed the associated functions of SNHG20/miR-197/LIN28 axis on OSCC proliferation and stemness. In summary, our results reveal the important function of SNHG20/miR-197/LIN28 axis in the oncogenesis and stemness of OSCC, suggesting the vital role of SNHG20 in OSCC tumorigenesis.