Epigallocatechin gallate (EGCG), as one of the main ingredients of green tea, has been reported to have potential prevention on a variety of solid tumors. However, the system-wide molecular mechanisms targeted to EGCG's anti-tumor effect have not been illustrated. Here, AGS and SGC7901 GC cells were used to investigate the EGCG-mediated change of gene expression. Our data showed that EGCG retarded cell growth and promoted cell death of GC in dose-dependent manner. Analyses based on transcription, translation as well as function were performed to explore the elusive anticancer role of EGCG. Of them, cell cycle was probably implicated key pathway of EGCG. Besides, our data revealed numerous LncRNAs activated after EGCG treatment. In this study, LINC00511 was discovered to be suppressed by EGCG and highly expressed in GC cells and tissues. Knockdown of LINC00511 inhibited cell growth and promoted cell death ratio in GC. Additionally, our data suggested LINC00511 could decrease the expression of miR-29b, followed by inducing GC development. Knockdown of miR-29b recovered the effects of LINC00511 silencing. In addition, we found overexpression of KDM2A, a target of miR-29b, would rescue the level of LINC00511. All the data showed that the LINC00511/miR-29b/KDM2A axis can be used as a diagnostic and therapeutic target for GC.

表没食子儿茶素没食子酸酯（EGCG）是绿茶的主要成分之一，据报道对多种实体瘤具有潜在的预防作用。然而，针对EGCG的抗肿瘤作用的全系统分子机制尚未阐明。在这里，AGS和SGC7901 GC细胞用于研究EGCG介导的基因表达变化。我们的数据表明，EGCG以剂量依赖的方式抑制了细胞的生长并促进了GC的细胞死亡。进行了基于转录，翻译和功能的分析，以探索EGCG难以捉摸的抗癌作用。其中，细胞周期可能与EGCG的关键途径有关。此外，我们的数据显示，EGCG处理后激活了许多LncRNA。在这项研究中，LINC00511被EGCG抑制并在GC细胞和组织中高表达。敲低LINC00511可抑制细胞生长并提高GC中的细胞死亡率。此外，我们的数据表明LINC00511可能会降低miR-29b的表达，然后诱导GC发育。沉默miR-29b恢复了LINC00511沉默的效果。此外，我们发现miR-29b的靶标KDM2A的过表达可以挽救LINC00511的水平。所有数据表明，LINC00511 / miR-29b / KDM2A轴可用作GC的诊断和治疗靶标。将挽救LINC00511的水平。所有数据表明，LINC00511 / miR-29b / KDM2A轴可用作GC的诊断和治疗靶标。将挽救LINC00511的水平。所有数据表明，LINC00511 / miR-29b / KDM2A轴可用作GC的诊断和治疗靶标。