School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Int J Oncol. 2022 Sep;61(3). doi: 10.3892/ijo.2022.5401. Epub 2022 Jul 29.
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.
舌鳞状细胞癌（TSCC）的预后较差，其 5 年总生存率并未显著改善。然而，TSCC 的确切分子机制仍知之甚少。通过 RNA 筛选，本研究鉴定了一种新型长非编码 RNA（lncRNA），角蛋白 16 假基因 6（lncKRT16P6），其在 TSCC 组织和细胞系中上调，并与 TSCC 肿瘤分期和分化等级相关。抑制 lncKRT16P6 的表达可降低 TSCC 细胞的迁移、侵袭和增殖能力。lncKRT16P6 可作为 microRNA（miR）-3180 的海绵，从而上调 GATA 锌指结构域包含 2A（GATAD2A）的表达。抑制 miR-3180 可逆转 lncKRT16P6 耗竭诱导的 TSCC 恶性程度降低，而 GATAD2A 耗竭可逆转 miR-3180 沉默诱导的 TSCC 恶性程度增强。综上所述，本研究揭示了一种潜在的竞争性内源性 RNA（ceRNA）调控途径，即 lncKRT16P6 通过结合 miR-3180 来调节 GATAD2A 的表达，最终促进 TSCC 的发生和转移。因此，lncKRT16P6 可作为 TSCC 临床干预的预后生物标志物和治疗靶点。
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