Abstract
In the present study, we investigated the potential effects of Isorhamnetin on the growth and metastasis of A549 human lung cancer cells, as well as the underlying mechanism. Treatment with Isorhamnetin exhibited a dose- and time-dependent inhibition on A549 cell proliferation. Furthermore, the cell adhesion and Transwell assay showed that treatment with Isorhamnetin (2.5, 5, and 10 μM) for 48 h resulted in a significant inhibition effect on cell adhesion, invasion and migration of A549 cells, depending on concentration, which was associated with the suppression of matrix metalloproteinase (MMP)-2 and MMP-9 activity and protein expression. Moreover, Isorhamnetin effectively suppressed the expressions of epithelial-to-mesenchymal transition (EMT) markers, as evidenced by the down-regulation of N-cadherin, vimentin and snail, as well as up-regulation of E-cadherin protein expression. Additionally, these inhibitions were mediated by interrupting AKT/ERK1/2 signaling pathways. Taken together, the results of the current study demonstrated that Isorhamnetin may become a good anti-metastastic agent against lung cancer A549 cell line by the suppression of EMT via interrupting Akt/ERK1/2 signaling pathway.
Highlights
Lung cancer is the most prominent causes of cancer-related mortality worldwide and the overall five years survival is approximately 15% [1,2]
Lung cancer invasion and metastasis are the primary factor for the failure of cancer treatment and for the poor prognosis of advanced non-small-cell lung cancer (NSCLC), which is responsible for its high mortality rates [21,22]
We examine the potential anti-metastasis effects of Isorhamnetin on A549 cells and the underlying mechanism involved
Summary
Lung cancer is the most prominent causes of cancer-related mortality worldwide and the overall five years survival is approximately 15% [1,2]. Of the lung cancer cases diagnosed, nearly 80% are non-small-cell lung cancer (NSCLC), which has a poor prognosis and limited therapeutic options, due to metastasis [3,4]. Cancer cell metastasis is the leading cause of cancer mortality and is a complex multistep process involving invasion and migration [5,6]. Local invasion and/or metastasis from primary sites to distant organs are responsible for the poor prognosis and treatment failure in patients with advanced NSCLC [7]. It is urgent to develop metastasis preventive strategies and to find new, safe and efficient preventive agents for the treatment of lung cancer
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