长非编码RNA与胃癌进展相关。对在线数据库分析发现LINC00346在胃癌（GC）组织中高表达，测序技术发现LINC00346在GC患者血清外泌体中表达较对照者上调。敲降LINC00346抑制胃癌细胞增殖及转移，下调CDK4、CD44、MET及ZEB1等表达。在线数据库分析发现转录因子（KLF5、MYC、JUN/FOS及SP1）绑定LINC00346启动子区。生物信息学发现LINC00346与miRNAs结合，敲低LINC00346上调相关miRNAs，RIP证实LINC00346与miRNA效应蛋白Ago2结合，CDK4、CD44、MET及ZEB1等是相应miRNAs靶基因。据此提出假设：促癌因子促进LINC00346表达，其通过竞争吸附相关miRNAs调控下游靶基因，促进胃癌进展。本课题组将利用生物信息学预测及实验验证相结合的方法证实上述假设，为GC早期诊断及分子靶向治疗提供依据。

Long non-coding RNA is closed related to the progression of gastric cancer (GC). We found that LINC00346 expression was significantly upregulated in GC tissues than in the adjacent normal tissues by analyzing Gene Expression Omnibus (GEO) database and it has been verified in collected tissues. We further found that LINC00346 expression was also remarkably elevated in exosomal RNA derived from serum of GC patients than that of health subjects by next generation sequencing technology. Knockdown of LINC00346 could significantly inhibit proliferation and metastasis of GC cell, and increase E-cadherin expression, decrease CDK4, CDK7, CD44, MET or ZEB1 expression. Cell cycle analysis revealed that inhibition of LINC00346 expression had an obvious cell-cycle arrest in GC cells. We found that LINC00346 promoter regions contained KLF5, MYC, JUN/FOS, and SP1 binding sites by analyzing GEO and ENCODE database. Bioinformatics was shown that LINC00346 could bind to miR-34a, miR-181c, miR-143, miR-340 and miR-205 with lower binding energy, and the above miRNAs were upregulted upon LINC00346 depletion. RNA immunoprecipitation assay was confirmed that LINC00346 binded to Argonaute2, the core subunits of RNA-induced silencing complex (RISC). CDK4, CDK7, CD44, MET or ZEB1 are the target genes of above miRNAs. Accordingly, the hypothesis is proposed: Oncogenic transcription factors promotes LINC00346 expression, and LINC00346 regulates CDK4, CDK7, CD44, MET or ZEB1 expression by competing for related miRNAs to promote the progression of GC.We will document this hypothesis by bioinformatic analysis and laboratory testing. Moreover, our work will further the understanding about the molecular mechanism of GC progression and provides a new basis of early diagnosis and molecular targeted therapy for GC.