β-elemene inhibited expression of DNA methyltransferase 1 through activation of ERK1/2 and AMPKα signalling pathways in human lung cancer cells: the role of Sp1.

摘要: β-elemene, a compound derived from Rhizoma zedoariae, is promising new plant-derived drug with broad-spectrum anticancer activity. However, the underlying mechanism by which this agent inhibits human lung cancer cell growth has not been well elucidated. In study, we showed that β-elemene non-small carcinoma (NSCLC) growth, and increased phosphorylation of ERK1/2, Akt AMPKα. Moreover, inhibited expression DNA methyltransferase 1 (DNMT1), was observed in presence specific inhibitors ERK (PD98059) or AMPK (compound C). Overexpression DNMT1 reversed effect on growth. Interestingly, metformin only but also strengthened β-elemene-reduced DNMT1. addition, suppressed Sp1 protein expression, eliminated either ERK1/2 inhibitor. Conversely, overexpression antagonized Taken together, our results show NSCLC via ERK1/2- AMPKα-mediated inhibition transcription factor Sp1, followed reduction expression. Metformin augments blockade signalling additively The reciprocal AMPKα pathways contribute to overall responses β-elemene. This study reveals potential novel cells.