肿瘤侵袭与转移是导致下咽癌患者预后差的关键原因。上皮-间质转化（EMT）是促进肿瘤转移的核心环节。课题组发现下咽癌组织中整合素α3呈异常高表达，且与肿瘤转移呈正相关；而下咽癌细胞整合素α3表达下调后，肿瘤转移潜能则明显减弱。最新研究发现具有显著EMT调控作用的Src/FAK信号级联可被整合素α3直接启动和放大。因此，课题组推测，整合素α3通过Src/FAK通路影响下咽癌的EMT和侵袭转移进程。本项目首先拟借助临床样本明确整合素α3对下咽癌转移的促进作用以及对Src/FAK信号活化影响；其次通过下咽癌细胞株和小鼠移植瘤模型，验证整合素α3促进肿瘤转移的功能；最后利用siRNA干扰、信号通路拮抗剂和过表达质粒等分子生物学方法，探究整合素α3调控下咽癌转移的具体分子机制。本研究旨在为阐明下咽癌转移新机制、形成治疗新靶点和可能的标志物提供理论依据和方法借鉴。

Tumor metastasis is the important cause of poor prognosis in hypopharyngeal cancer. Epithelial-mesenchymal transition (EMT) is the key point leading to tumor metastasis. Our preliminary experiments found that the expression of integrin α3 in tumor tissues of hypopharyngeal cancer was abnormally high，and positively correlated with tumor metastasis. After knockdown of integrin α3 in hypopharyngeal cancer cells，the metastasis ability of tumor cells in vitro was inhibited. Recent discoveries suggest that the Src/FAK signaling pathway plays an important role in tumor EMT. While integrin α3 is an important regulator of the Src/FAK pathway. Therefore, we hypothesize that integrin α3 regulate the EMT of hypopharyngeal cancer via the Src/FAK pathway. In this study, we firstly aim to further verify the clinical correction between the expression of integrin α3 and hypopharyngeal cancer metastasis with clinical specimens. Then the role of integrin α3 in promoting tumor metastasis was analyzed by in vitro model of hypopharyngeal cancer cell and transplanted tumor in mice. Finally, molecular biological methods such as siRNA interference, signaling pathway antagonists and overexpression of plasmids were used to explore the specific molecular mechanism of integrin α3 regulating hypopharyngeal cancer metastasis. To provide a new marker for the metastasis of hypopharyngeal cancer and a new target for the treatment of hypopharyngeal cancer metastasis.