外泌体miRNAs与肿瘤发展有关，但在肺腺癌侵袭转移中的作用及分子机制尚无明确。我们前期发现：exosomal-miR-1260b在肺腺癌患者术前血浆中表达升高且术后降低。体外细胞共培养和transwell实验证实exosomal-miR-1260b参与肿瘤细胞间的通讯，并可促进细胞侵袭。qRT-PCR和western blot发现miR-1260b可下调Wnt/β-catenin通路的拮抗因子sFRP1、Smad4的表达。因此，我们提出外泌体介导的肿瘤细胞间的通讯将exosomal-miR-1260b转运至周围肿瘤细胞，下调sFRP1、Smad4表达，活化Wnt/β-catenin通路，从而增强该细胞侵袭转移能力，最终促进肺腺癌侵袭转移的假说。我们拟从临床、体外细胞、动物模型三个层面探讨exosomal-miR-1260b调控肺腺癌侵袭转移的作用及分子机制，为肺腺癌的临床诊治提供新线索。

Exosomal-miRNAs are closely related to tumor development, while the role and molecular mechanism in lung adenocarcinoma (LAC) remains uncertain. Quantitative RT-PCR showed that exosomal-miR-1260b was increased in the preoperative plasma and decreased in the postoperative plasma of patients with LAC. In vitro, co-cultivation assay demonstrated that exosomal-miR-1260b was involved in cell-cell communication. Meanwhile, transwell assay revealed that exsomal-miR-1260b promoted the invasion of LAC cells. Furthermore, qRT-PCR and western blot indicated that miR-1260b down-regulated the expression levels of sFRP1 and Smad4 genes, which are inhibitors of Wnt/β-catenin signaling pathway. Thus, we hypothesized that exosome-mediated transfer of miR-1260b might promote the invasion and metastasis of LAC by down-regulating sFRP1 and Smad4 and subsequently activating Wnt/β-catenin signaling pathway. To identify this hypothesis, employing human sample, cell and molecule, NOD/SCID mice model, we will investigate the role and molecular mechanism of exosomal-miR-1260b in the invasion and metastasis of LAC, which will offer new clues into the clinical diagnosis and treatment for LAC.