肿瘤转移和复发是肺腺癌预后差的主要原因。长链非编码RNA（lncRNA）在肺癌转移和肺癌干细胞自我更新中扮演重要角色，其可直接与信号蛋白的功能域结合，调控蛋白磷酸化，从而调节下游信号转导。我们前期报道SOX5参与调节肺腺癌转移且在肺腺癌中高表达，进一步研究发现STAT3是SOX5的上游转录因子，参与调控肺腺癌转移和干性维持。肺腺癌转录组测序数据分析结果显示，lncRNA FAM83A-AS1在肺腺癌中显著高表达，与SOX5的表达呈正相关。体外实验证明FAM83A-AS1调控STAT3活化和SOX5的表达。本项目拟通过肺腺癌临床样本研究、裸鼠成瘤及转移模型研究和细胞学功能及机制分析，揭示FAM83A-AS1通过与JAK2-STAT3结合促进STAT3活化和入核，进而转录激活SOX5表达，促进肺腺癌转移和干细胞自我更新。本研究旨在丰富肺腺癌发病机制，为肺腺癌治疗提供新的线索和科学依据。

Tumor recurrence and metastasis are the major causes of poor prognosis of lung adenocarcinoma (LAC). Long non-coding RNA (lncRNA) plays an important role in lung cancer metastasis and tumor-initiating cell self-renewal. Our previous study showed that SOX5 promoted LAC metastasis and was highly expressed in LAC tissues. Furthermore, we found that STAT3, an upstream transcriptional factor of SOX5, played an important role in LAC metastasis and stemness maintenance. Here we discovered that lncRNA FAM83A-AS1 is highly expressed in LAC tissues. The expression level of FAM83A-AS1 is correlated with SOX5 expression. In this proposal, we aim to clarify the mechanism how FAM83A-AS1 regulates STAT3 phosphorylation, activating SOX5 transcription and LAC metastasis and stemness using clinical study, nude mice xenograft model, and in vitro functional and mechanistic analysis. This study will provide new therapeutic evidences for indentifying a novel pathogenesis of lung adenocarcinoma.