The upregulation of Myb and Peg3 may mediate EGCG inhibition effect on mouse lung adenocarcinoma

Abstract

The antioxidant activity of green tea polyphenol epigallocatechin-3-gallate (EGCG) has been found to be critical in inhibiting carcinogenesis. In our previous study, we 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. In this study, we further conducted some statistical analysis on our microarray data and employed The Cancer Genome Atlas (TCGA) lung adenocarcinoma datasets as additional control. We postulated 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. With this assumption, we identified Myb and Peg3 as the primary genes involved in the cancer inhibitory activities of EGCG.