The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from Antrodia cinnamomea (EEAC) on
lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine
tumor model were separately used to examine cell migration,
protein expression, and
tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing
proteins,
adenosine 5'-monophosphate-activated
protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting
proteins,
protein kinase B (Akt), mammalian tarfet of
rapamycin (mTOR), extracellular signal-regulating
kinase 1/2 (ERK1/2),
retinoblastoma protein (Rb),
cyclin E, and
cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of
gelatinases. In addition, our data showed that
tumor growth was suppressed
after treatment with EEAC in a murine allograft
tumor model. Some bioactive compounds from EEAC, such as
cordycepin and
zhankuic acid A, were demonstrated to reduce the
protein expressions of
matrix metalloproteinase (MMP)-9 and
cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to
paclitaxel by reducing the
protein levels of
caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of
lung cancer.