lncKRT16P6 promotes tongue squamous cell carcinoma progression by sponging miR‑3180 and regulating GATAD2A expression
- Mi Zhang
- Ling Wu
- Xudong Wang
- Jiang Chen
Affiliations: School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China
- Published online on: July 28, 2022 https://doi.org/10.3892/ijo.2022.5401
Copyright: © Zhang
et al. This is an open access article distributed under the
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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 expression reduced TSCC cell migration, invasion and proliferation. lncKRT16P6 sponged microRNA (miR)‑3180 and upregulated 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 modulates 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.