Abstract
Resveratrol (RSV), a health-promoting natural product, has been shown to affect various cellular processes in tumor cells. However, the specific protein targets of RSV and the mechanism of action (MOA) of its anticancer effect remain elusive. In this study, the pharmacological activity of RSV was first evaluated in A549 cells, and the results showed that RSV significantly inhibited A549 cell migration but did not affect cell viability. To elucidate the underlying mechanism, a quantitative chemical proteomics approach was employed to identify the protein targets of RSV. A total of 38 target proteins were identified, and proteomic analysis showed that the targets were mainly involved in cytoskeletal remodeling and EMT, which were verified by subsequent in vitro and in vivo assays. In conclusion, RSV inhibits A549 cell migration by binding to multiple targets to regulate cytoskeletal remodeling and suppress EMT.
Highlights
Lung cancer has become one of the critical causes of cancer death throughout the world due to the prevalent complication of apoptosis resistance against different anticancer agents (Ramezanpour et al, 2014)
A trans-well assay was performed to evaluate the effect of RSV on A549 cell invasion, and we found that RSV remarkably suppressed A549 cell invasion in a dose-dependent manner (Figure 1E)
Many studies have shown that RSV inhibits human A549 lung cells by affecting a variety of cellular processes, including the cell cycle (Yuan et al, 2015), apoptosis (Kim et al, 2003), autophagy (Hu et al, 2016), mitochondrial dysfunction (Gu et al, 2016), invasion and metastasis (Wang et al, 2013), depending on different experimental conditions and systems
Summary
Lung cancer has become one of the critical causes of cancer death throughout the world due to the prevalent complication of apoptosis resistance against different anticancer agents (Ramezanpour et al, 2014). Reports have shown that RSV affects a large variety of cellular processes in lung cancer cells, including the cell cycle (Abe et al, 2010; Yuan et al, 2015), mitochondrial function (Gu et al, 2016), oxidative stress (Gu et al, 2015), and epithelialto-mesenchymal transition (Wang et al, 2013), to inhibit cell proliferation and migration. These findings expand our understanding of the role of RSV in lung cancer cells, but the exact mechanism is not clear. The specific target proteins of RSV in lung cancer cells remain elusive, increasing the difficulty of mechanistic elucidation and new therapeutic target discovery (Chen et al, 2017b)
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