Effects of maslinic acid on the proliferation and apoptosis of A549 lung cancer cells

Bai,Xue; Zhang,Yi; Jiang,Hongfang; Yang,Peng; Li,Hui; Zhang,Yue; He,Ping

doi:10.3892/mmr.2015.4552

Effects of maslinic acid on the proliferation and apoptosis of A549 lung cancer cells

Authors:
- Xue Bai
- Yi Zhang
- Hongfang Jiang
- Peng Yang
- Hui Li
- Yue Zhang
- Ping He
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Affiliations: Department of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China
Published online on: November 11, 2015 https://doi.org/10.3892/mmr.2015.4552
Pages: 117-122
Copyright: © Bai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Maslinic acid (MA) is a pentacyclic triterpene acid that is present in numerous dietary plants. Although certain studies have demonstrated that MA has anti‑cancer properties in different cell types, the effect of MA on lung cancer cell proliferation and apoptosis and the potential underlying mechanisms remain to be elucidated. In the present study, A549 lung cancer cells were treated with different doses of MA and it was found that MA significantly inhibited A549 cell growth in a dose‑dependent manner. In addition, Annexin V/propidium iodide flow cytometric analysis demonstrated that MA induced apoptosis of A549 cells. The present study also confirmed that MA induced apoptosis by observing morphological alterations. In addition, the effect of MA treatment on the levels of apoptosis‑associated proteins was examined. The results demonstrated that MA treatment suppressed the expression of caspase‑3, ‑8 and ‑9, and increased the expression of cleaved caspase‑3, ‑8 and ‑9 in a dose‑dependent manner. The level of inhibitors of apoptosis (IAPs) and Smac, which are possible upstream factors of caspase proteins, were also examined. It was found that MA treatment increased the protein expression of Smac and decreased the protein levels of c‑IAP1, c‑IAP2, X‑linked inhibitor of apoptosis protein (XIAP) and Survivin in a dose‑dependent manner. These results suggested that MA inhibited proliferation and induced apoptosis of A549 cells through regulation of caspase cleavage as well as Smac, c-IAP1, c-IAP2, XIAP and Survivin.

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