Tongue squamous cell carcinoma (TSCC) is the most common oral malignancy. Previous studies found that microRNA (miR)-26a and miR-26b were downregulated in TSCC tissues. The current study was designed to explore the effects of miR-26a/miR-26b on TSCC progression and the potential mechanism. Expression of miR-26a, miR-26b and p21 Activated Kinase 1 (PAK1) in TSCC tissues and cell lines was detected by reverse transcription- quantitative polymerase chain reaction (RT-qPCR). Flow cytometry analysis was performed to examine cell cycle and apoptosis. Transwell assay was conducted to evaluate the migrated and invasive abilities of SCC4 and Cal27 cells. In addition, western blot assay was employed to analyze the protein level. Glucose assay kit and lactate assay kit were utilized to analyze glycolysis. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were applied to explore the relationship between miR-26a/miR-26b and PAK1. Xenograft tumor model was constructed to explore the role of miR-26a/miR-26b in vivo. Both miR-26a and miR-26b were underexpressed, while PAK1 was highly enriched in TSCC. Overexpression of miR-26a and miR-26b inhibited TSCC cell cycle, migration invasion and glycolysis, while promoted cell apoptosis. Both miR-26a and miR-26b directly targeted and negatively regulated PAK1 expression. Introduction of PAK1 partially reversed miR-26a/miR-26b upregulation-mediated cellular behaviors in TSCC cells. Gain of miR-26a/miR-26b blocked TSCC tumor growth in vivo. MiR-26a/miR-26b repressed TSCC progression via targeting PAK1 in vitro and in vivo, which enriched our understanding about TSCC development and provided new insights into the its treatment.

中文翻译：

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MiR-26a/miR-26b 通过靶向 PAK1 抑制舌鳞状细胞癌进展

舌鳞状细胞癌（TSCC）是最常见的口腔恶性肿瘤。先前的研究发现，microRNA (miR)-26a 和 miR-26b 在 TSCC 组织中下调。本研究旨在探讨 miR-26a/miR-26b 对 TSCC 进展的影响及其潜在机制。通过逆转录-定量聚合酶链反应 (RT-qPCR) 检测 TSCC 组织和细胞系中 miR-26a、miR-26b 和 p21 活化激酶 1 (PAK1) 的表达。进行流式细胞术分析以检查细胞周期和细胞凋亡。进行 Transwell 测定以评估 SCC4 和 Cal27 细胞的迁移和侵袭能力。此外，采用蛋白质印迹法分析蛋白质水平。葡萄糖测定试剂盒和乳酸测定试剂盒用于分析糖酵解。应用双荧光素酶报告基因和 RNA 免疫沉淀 (RIP) 测定来探索 miR-26a/miR-26b 和 PAK1 之间的关系。构建异种移植肿瘤模型以探索miR-26a/miR-26b在体内的作用。miR-26a 和 miR-26b 均低表达，而 PAK1 在 TSCC 中高度富集。miR-26a和miR-26b的过表达抑制TSCC细胞周期、迁移侵袭和糖酵解，同时促进细胞凋亡。miR-26a 和 miR-26b 都直接靶向并负调控 PAK1 表达。PAK1 的引入部分逆转了 TSCC 细胞中 miR-26a/miR-26b 上调介导的细胞行为。miR-26a/miR-26b 的增加阻止了体内 TSCC 肿瘤的生长。MiR-26a/miR-26b 通过在体外和体内靶向 PAK1 抑制 TSCC 进展，