Abstract
Epigallocatechin-3-gallate (EGCG), a green tea–derived polyphenol, exhibits antitumor activities. An EGCG nanoemulsion (nano-EGCG) was prepared to improve the stability and reduce the side effects of EGCG for treatment of human lung cancer cells, and the antitumor effects were studied. The possible molecular mechanism underlying its antitumor effects on cultured human lung cancer cells was also elucidated. The antitumor effects of EGCG and nano-EGCG were determined using methylthiazolyldiphenyl-tetrazolium bromide (MTT), colony formation, migration, and invasion assays. In addition, changes in the AMP-activated protein kinase (AMPK) signaling pathway were investigated using Western blot analyses. AMPK inhibitors were used to determine the roles of the AMPK signaling pathway involved in the molecular mechanism of the nano-EGCG. Our results showed that both EGCG and nano-EGCG inhibited the growth of H1299 lung cancer cells, with half-maximal inhibitory concentrations of 36.03 and 4.71 μM, respectively. Additionally, nano-EGCG effectively suppressed lung cancer cell colony formation, migration, and invasion in a dose-dependent manner. Nano-EGCG may inhibit lung cancer cell invasion through matrix metalloproteinase (MMP)-2- and MMP-9-independent mechanisms. Furthermore, the expression of several key regulatory proteins in the AMPK signaling pathway was modulated by nano-EGCG. Nano-EGCG may inhibit lung cancer cell proliferation, colony formation, migration, and invasion through the activation of AMPK signaling pathways. This novel mechanism of nano-EGCG suggests its application in lung cancer prevention and treatment. Our results provide an experimental foundation for further research on its potential activities and effects in vivo.
Highlights
Lung cancer is established globally to be the leading cause of cancer-related mortality
To study the effects of EGCG and nano-EGCG on human lung cancer cells, we first determined whether EGCG or nano-EGCG at the indicated concentrations of treatments for 24, 48, and 72 hours could influence the viabilities of H1299, A549, and BEAS2B cells
We discovered that EGCG could suppress H1299 cell proliferation at doses higher than 20 μM
Summary
Lung cancer is established globally to be the leading cause of cancer-related mortality. Executed research has detected LKB1 mutations in inherited cancer disorders and lung cancers, which suggests that AMPK plays a role in tumour suppression[5,6]. In patients with NSCLC, high expression of phosphorylated AMPK was reported to be strongly associated with the lengthening of recurrence-free and overall survival[8]. Evidence suggests that mutations in LKB1 may lead to unsuppressed cell proliferation because of the inability to activate AMPK in response to the tumor[9]. EGCG can inhibit the growth of small-cell lung cancer cells, it exhibits variable effects on the small number of NSCLC cell lines tested[17,18]. In our study, an EGCG nanoemulsion (nano-EGCG) was prepared, and the antitumour effects exerted on human lung cancer cells by the prepared nano-EGCG were investigated. The underlying molecular mechanisms of nano-EGCG in lung cancer cells were identified
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