据报道，Wiskott-Aldrich 综合征蛋白家族 Verprolin 同源结构域蛋白 3 (WAVE3) 是一种在多种恶性肿瘤中调节细胞增殖和运动的癌基因，但其在舌鳞状细胞癌 (TSCC) 中的作用仍不清楚。本研究旨在探讨WAVE3在TSCC中的表达及机制。我们招募了 2013 年 6 月至 2014 年 2 月期间入院的 64 名 TSCC 患者，收集他们的癌组织和癌旁正常组织，通过免疫组织化学测定 WAVE3 的表达。分析WAVE3表达与TSCC患者病理特征的相关性。然后，进行了7年的随访，观察WAVE3在评估患者预后方面的价值。此外，购买人TSCC SCC9、SCC25和CAL27细胞，通过Cell Counting Kit-8 (CCK-8)、Transwell和划痕实验检测其增殖、侵袭和迁移能力，同时实时定量PCR (qRT-PCR) 和蛋白质印迹分别用于量化 WAVE3 和上皮间质转化 (EMT) 相关蛋白的表达。选择最活跃的细胞系，用沉默WAVE3（命名为WAVE3-sh组）和过表达WAVE3 cDNA（命名为WAVE3-OE组）的慢病毒载体感染，观察干扰WAVE3表达对TSCC细胞生物学行为的影响。 TSCC组织中WAVE3的阳性表达明显增强，且主要位于细胞质。此外，WAVE3与T分期、临床分期、淋巴结转移、远处转移和分化程度之间存在密切相关性（P<0.05）。后续分析表明，WAVE3 表达增加预示着死亡风险升高 (P < 0.05)。在所研究的各种TSCC细胞系中选择SCC9进行后续实验，因为它表现出最强的增殖、侵袭和迁移能力（P < 0.05）。沉默SCC9细胞中WAVE3的表达会降低细胞增殖、侵袭、迁移和EMT相关蛋白的表达（P<0.05），而增加WAVE3的表达会促进SCC9的活力。 WAVE3在TSCC中高表达，促进肿瘤细胞的EMT，加速其增殖、侵袭和迁移，这可能为未来TSCC的分子靶向治疗提供新的理论基础。© 2023。作者，获得 Springer Science Business Media, LLC（Springer Nature 旗下公司）的独家许可。

Wiskott-Aldrich syndrome protein family verprolin-homologous domain-containing protein 3 (WAVE3) is reported as an oncogene regulating cell proliferation and motility in multiple malignancies, while its role in tongue squamous cell carcinoma (TSCC) remains unknown. This study aimed to explore the expression and mechanism of WAVE3 in TSCC. We enrolled 64 TSCC patients admitted between June 2013 and February 2014 and collected their cancerous and adjacent normal tissues to determine WAVE3 expression by immunohistochemistry. The correlation of WAVE3 expression with TSCC patients' pathological characteristics was analyzed. Then, a 7-year follow-up was conducted to observe the value of WAVE3 in evaluating patient outcomes. In addition, human TSCC SCC9, SCC25, and CAL27 cells were purchased and detected by Cell Counting Kit-8 (CCK-8), Transwell, and scratch-wound assays for their proliferation, invasion, and migration capacities, while real-time quantitative PCR (qRT-PCR) and Western blotting were utilized to quantify WAVE3 and epithelial-mesenchymal transition (EMT)-related protein expression, respectively. The most active cell lines were selected to be infected with lentiviral vectors that silenced WAVE3 (named WAVE3-sh group) and overexpressed WAVE3 cDNA (named WAVE3-OE group) to observe the impacts of interfering WAVE3 expression on TSCC cell biological behavior. The positive expression of WAVE3 in TSCC tissue was found to be obviously enhanced and predominantly located in the cytoplasm. In addition, close correlations were identified between WAVE3 and T staging, clinical staging, lymphatic metastasis, distant metastasis, and differentiation degree (P < 0.05). Increased WAVE3 expression predicted an elevated risk of death, as indicated by the follow-up analysis (P < 0.05). SCC9 was selected for subsequent experiments among various TSCC cell lines studied because it showed the most potent ability to proliferate, invade, and migrate (P < 0.05). Silencing WAVE3 expression in SCC9 cells decreased cell proliferation, invasion, migration, and EMT-related protein expression (P < 0.05), while increasing WAVE3 expression promoted SCC9 viability. WAVE3, which was highly expressed in TSCC, promoted EMT in tumor cells and accelerated their proliferation, invasion, and migration, which might provide a new theoretical basis for molecular targeted therapy of TSCC in the future.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.