口腔鳞状细胞癌（OSCC）是头颈部鳞状细胞癌的主要类型之一。尽管在治疗OSCC方面取得了进展，但它仍然对人类健康构成威胁，并需要创新的治疗策略以延长OSCC患者的寿命。本研究旨在评价骨髓基质抗原2（BST2）和STAT1是否是OSCC的潜在治疗靶点。使用小干扰RNA（siRNA）或过表达质粒调节BST2或STAT1的表达。进行Western blot和反转录定量PCR以评估信号通路成分的蛋白质和mRNA表达水平的变化。使用划痕实验，Transwell实验和体外集落形成实验评估BST2和STAT1表达变化对OSCC细胞的迁移，侵袭和增殖的影响。使用细胞来源的异种移植模型评估BST2和STAT1对OSCC发生和发展的影响。最后，证明BST2表达在OSCC中明显上调，并且高表达的BST2促进了OSCC细胞的转移，侵袭和增殖。此外，证明了BST2的启动子区域是由转录因子STAT1调节的，并且STAT1 / BST2轴可通过AKT / ERK1 / 2信号通路影响OSCC的行为。体内研究还表明，STAT1下调通过AKT / ERK1 / 2信号通路下调BST2表达抑制了OSCC生长。

Oral squamous cell carcinoma (OSCC) is one of the main types of head and neck squamous cell carcinoma. Although progress has been made in treating OSCC, it remains a threat to human health, and novel therapeutic strategies are needed to extend the lifespan of patients with OSCC. The present study, evaluated whether bone marrow stromal antigen 2 (BST2) and STAT1 were potential therapeutic targets in OSCC. Small interfering RNA (siRNA) or overexpression plasmids were used to regulate BST2 or STAT1 expression. Western blotting and reverse transcription‑quantitative PCR were performed to assess changes in the protein and mRNA expression levels of signaling pathway components. The effects of BST2 and STAT1 expression changes on the migration, invasion and proliferation of OSCC cells were assessed using the scratch test assay, Transwell assay and colony formation assay in vitro, respectively. Cell‑derived xenograft models were used to evaluate the impact of BST2 and STAT1 on the occurrence and development of OSCC in vivo. Finally, it was demonstrated that BST2 expression was significantly upregulated in OSCC. Furthermore, it was demonstrated that high expression of BST2 in OSCC contributed to the metastasis, invasion and proliferation of OSCC cells. Moreover, it was demonstrated that the promoter region of BST2 was regulated by the transcription factor STAT1, and that the STAT1/BST2 axis could affect the behavior of OSCC via the AKT/ERK1/2 signaling pathway. In vivo studies also demonstrated that STAT1 downregulation inhibited OSCC growth by down‑regulating BST2 expression via the AKT/ERK1/2 signaling pathway.