The up-regulation of Myb may help mediate EGCG inhibition effect on mouse lung adenocarcinoma

Green tea polyphenol epigallocatechin-3-gallate (EGCG) has been demonstrated to inhibit cancer in experimental studies through its antioxidant activity and modulations on cellular functions by binding specific proteins. By means of computational analysis and functional genomic approaches, we previously identified a set of protein coding genes and microRNAs whose expressions were significantly modulated in response to the EGCG treatment in tobacco carcinogen-induced lung adenocarcinoma in A/J mice. However, to what degree these genes are involved in the cancer inhibition of EGCG remains unclear.

In this study, we further employed statistical methods and literature research to analyze these data in combination with The Cancer Genome Atlas (TCGA) lung adenocarcinoma datasets for additional data mining. Under the assumption that, if a gene mediates EGCG's cancer inhibition, its expression level change caused by EGCG should be opposite to what occurred in the carcinogenesis, we identified Myb and Peg3 as the primary putative genes involved in the cancer inhibitory activity. Further analysis suggested that the regulation of Myb could be mediated through an EGCG-upregulated microRNA, miR-449c-5p.

Although the actions of EGCG involve multiple targets/pathways, further analysis by mining the existing genomic datasets revealed that the upregulations of Myb and Peg3 are likely the key anti-cancer events of EGCG in vivo.