RESUMO
Emodin is a natural anthraquinone extract of Chinese medicinal herbs. Several studies demonstrated the antitumor activity of this extract, particularly for lung cancer. However, the mode of action of emodin remains obscure. In this study we evaluated in vitro and in vivo anti-lung cancer properties of emodin in human lung adenocarcinomas and the underlying molecular mechanism involved. Our results demonstrated emodin caused a significant inhibition of cell viability and induced apoptosis in lung cancer cells to a level that is relative to that of normal epithelial cells. Furthermore, RNA-seq transcriptome analysis revealed 65 common genes(>2-fold change) with a significant expression in A549, and H1650 cells under emodin treatment. In vitro qRT-PCR results confirmed that 4 genes (ATP6V0D2, C11orf96, TIPARP, and CDKN1A) were up-regulated, and 9 genes (TNFSF10, IFIT1, EGLN3, RCOR2, ARRB1, FLVCR2, BAIAP2-DT, FAM111B, and TGFB2) were down-regulated in A549 and H1650 adenocarcinoma cell lines. The in vivo experiment demonstrated emodin could significantly decrease tumor volume and tumor weight of mice compared with the control group. However, emodin treatment has no obvious effect on body weight of mice. Moreover, in vivo qRT-PCR results revealed that 3 genes (ATP6V0D2, C11orf96, and TIPARP) were up-regulated, and 6 genes (TNFSF10, IFIT1, EGLN3, BAIAP2-DT, FAM111B, and TGFB2) were down-regulated in tumor tissues compared with the control group. These findings suggested that emodin could help treat lung cancer and has a potential for further investigations as an anti-lung cancer drug.