lncKRT16P6 promotes tongue squamous cell carcinoma progression by sponging miR-3180 and regulating GATAD2A expression

Abstract

Tongue squamous cell carcinoma (TSCC) is characterized by a poor prognosis and its 5-year overall survival rate has not improved significantly. However, the precise molecular mechanisms underlying TSCC remain largely unknown. Through RNA screening, the present study identified a novel long noncoding RNA (lncRNA), keratin 16 pseudogene 6 (lncKRT16P6), which was upregulated in TSCC tissues and cell lines and associated with TSCC tumor stage and differentiation grade. Inhibition of lncKRT16P6 expres- sion reduced TSCC cell migration, invasion and proliferation. lncKRT16P6 sponged microRNA (miR)-3180 and upregu- lated GATA zinc finger domain containing 2A (GATAD2A) expression. miR-3180 inhibition reversed the lncKRT16P6 depletion-induced attenuation of TSCC malignancy and GATAD2A depletion reversed the miR-3180 silencing-induced enhancement of TSCC malignancy. In summary, the present study revealed a potential competitive endogenous RNA (ceRNA) regulatory pathway in which lncKRT16P6 modu- lates GATAD2A expression by binding miR-3180, ultimately promoting tumorigenesis and metastasis in TSCC. Therefore, lncKRT16P6 may be used as a prognostic biomarker and therapeutic target for clinical intervention in TSCC.