Background: Head and neck squamous cell carcinoma (HNSCC) features aggressive progression and a complex immunosuppressive microenvironment, contributing to poor patient prognosis and highlighting the need to identify key molecular drivers. The actin‑binding protein PLS3 (Plastin‑3) is involved in tumor metastasis, yet its expression, function, and therapeutic potential in HNSCC remain unclear. Methods: PLS3 expression was analyzed via polymerase chain reaction (PCR), Western blot (WB), and immunohistochemistry (IHC). PLS3 was knocked down in vitro to assess its effects on HNSCC cell functions, and in vivo models were established to evaluate tumor progression and immune microenvironment. Bioinformatics analyses explored the relationship between PLS3 and tumor immunity. Results: PLS3 was upregulated in HNSCC tissues and correlated with adverse clinical outcomes. Knockdown of PLS3 inhibited cell proliferation, migration, and invasion in vitro, and suppressed tumor growth in vivo. Mechanistically, PLS3 promoted HNSCC progression by activating the epithelial-mesenchymal transition (EMT) program. Bioinformatics and animal studies further linked PLS3 overexpression to an immunosuppressive microenvironment characterized by reduced CD8+ T-cell infiltration and downregulated chemokine expression. Conclusions: This study elucidates the oncogenic role of PLS3 in HNSCC and supports its potential as a prognostic biomarker and therapeutic target.
背景：头颈部鳞状细胞癌（HNSCC）具有进展侵袭性强和免疫抑制微环境复杂的特点，导致患者预后不良，凸显了识别关键分子驱动因素的必要性。肌动蛋白结合蛋白PLS3（Plastin-3）参与肿瘤转移，但其在HNSCC中的表达、功能及治疗潜力尚不明确。方法：通过聚合酶链式反应（PCR）、蛋白质印迹法（WB）和免疫组织化学（IHC）分析PLS3的表达。在体外敲低PLS3以评估其对HNSCC细胞功能的影响，并建立体内模型以评估肿瘤进展和免疫微环境。通过生物信息学分析探讨PLS3与肿瘤免疫的关系。结果：PLS3在HNSCC组织中表达上调，并与不良临床结局相关。敲低PLS3在体外抑制细胞增殖、迁移和侵袭，在体内抑制肿瘤生长。机制上，PLS3通过激活上皮-间质转化（EMT）程序促进HNSCC进展。生物信息学分析和动物研究进一步表明，PLS3过表达与免疫抑制微环境相关，其特征为CD8+ T细胞浸润减少和趋化因子表达下调。结论：本研究阐明了PLS3在HNSCC中的致癌作用，并支持其作为预后生物标志物和治疗靶点的潜力。
肿瘤(癌症)患者之家