[No authors listed]
Cancer cell invasion and metastasis are the leading causes of the high mortality rates in patients with malignant tumors. There is accumulating evidence to indicate that dysregulated long nonâcoding RNAs (lncRNAs) may be involved in the progression of tumor invasion and metastasis. However, the regulatory mechanisms of the aberrant expression of lncRNAs remain largely unknown, although the roles of lncRNAs as drivers of tumor suppressive and oncogenic functions have appeared in prevalent cancer types in recent years. In the present study, we identified that the transcription factor, activating enhancerâbinding protein 4 (TFAP4), acts as a key modulator of translation regulatory long nonâcoding RNA which has been proven to promote the invasion and metastasis of gastric cancer (GC) cells. We revealed that was upregulated in gastric carcinogenesis and promoted cell migration and invasion in GC. Using bioinformatics analysis, we observed that there were several potential binding sites of TFAP4 in the promoter region of The knockdown of TFAP4 significantly reduced the expression level of whereas the ectopic expression of TFAP4 significantly increased the expression level of Tduanyu1795NA1 in GC cell lines. Dual luciferase reporter assay combined with chromatin immunoprecipitation (ChIP) revealed that TFAP4 specifically regulated the transcriptional activity of Tduanyu1795NA1 by binding to the Eâbox motifs in the Tduanyu1795NA1 promoter. In addition, there was a positive correlation between the TFAP4 and Tduanyu1795NA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of Tduanyu1795NA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.
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