转移是肺癌临床治疗失败主要原因。上皮间质转化是肿瘤转移中关键事件。我们前期研究发现，整合素α6（ITGA6）表达水平升高促进肺癌细胞上皮间质转化、侵袭转移，但其机制仍不清楚。MicroRNA是基因表达调控的重要因素。根据生物信息学分析和荧光素酶报告基因活性检测结果，我们提出miR-32可能通过调控ITGA6表达，抑制肺癌细胞上皮间质转化，进而抑制肺癌转移的推测。本研究拟分析miR-32、ITGA6的表达水平的相关性以及与肺癌患者临床病理参数、预后的相关性，在细胞和组织水平研究ITGA6是否是miR-32靶基因，通过体内外实验研究miR-32调控ITGA6表达，抑制肺癌细胞上皮间质转化、转移的分子机制，探讨miR-32新的作用靶点及在肿瘤转移相关信号通路中的作用机制，为临床防治肺癌转移提供新的分子标志和潜在的重要靶点。

Metastasis is the major cause of treatment failure in lung cancer patients. Epithelial mesenchymal transition (EMT) is a critical early event for many carcinomas metastasis. In our previous study, we found integrin alpha6 (ITGA6) overexpression could promote lung cancer cell EMT, invasion and metastasis. However, the mechanism involved in this process is still not clear. MicroRNAs are important post-transcriptional regulators of their target genes. Bioinformatics analysis and luciferase reporter gene assay showed that ITGA6 gene may be a potential target gene of miR-32. Therefore, we hypothesize miR-32 could regulate the expression of ITGA6, trigger the EMT, and lead to the occurrence of tumor metastasis in lung cancer. This project aims to analyze the correlation of miR-32 with the expression levels of ITAG6 and with clinicopathological and prognostic parameters in lung cancer, study whether ITGA6 is the target gene miR-32 at the cell and tissue level, and focus on possible molecular mechanism that ITGA6 is regulated by miR-32 in lung cancer EMT and metastasis in vitro and in vivo to further provide new evidence for miR-32 new gene targets and the role of miR-32 in lung cancer novel metastasis-related signaling, and provide lung cancer novel metastasis-related molecular markers and potential important targets.