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Int. J. Mol. Sci. 2018, 19(3), 791; doi:10.3390/ijms19030791

Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model

School of Pharmacy, China Medical University, Taichung 40402, Taiwan
School of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan
Department of Pathology, Taichung Hospital, Ministry of Health and Welfare Taiwan, Taichung 40343, Taiwan
Department of Healthcare Administration, Asia University, Taichung 41354, Taiwan
Author to whom correspondence should be addressed.
Received: 11 January 2018 / Revised: 18 February 2018 / Accepted: 6 March 2018 / Published: 9 March 2018
(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention)
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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. View Full-Text
Keywords: Antrodia cinnamomea; anti-migration; anti-proliferation; paclitaxel resistance; lung cancer Antrodia cinnamomea; anti-migration; anti-proliferation; paclitaxel resistance; lung cancer

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Wu, C.-H.; Liu, F.-C.; Pan, C.-H.; Lai, M.-T.; Lan, S.-J.; Wu, C.-H.; Sheu, M.-J. Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model. Int. J. Mol. Sci. 2018, 19, 791.

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