α-Chaconine-reduced Metastasis Involves a PI3K/Akt Signaling Pathway with Downregulation of NF-κB in Human Lung Adenocarcinoma A549 cells
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文摘
α-Chaconine, isolated from Solanum tuberosum Linn., is a naturally occurring steroidal glycoalkaloid in potato sprouts. Some reports demonstrated that α-chaconine had various anticarcinogenic properties. The aim of this study is to investigate the inhibitory effect of α-chaconine on lung adenocarcinoma cell metastasis in vitro. We chosed the highly metastatic A549 cells, which were treated with various concentrations of α-chaconine to clarify the potential of inhibiting A549 cells invasion and migration. Data showed that α-chaconine inhibited A549 cell invasion/migration according to wound healing assay and Boyden chamber assay. Our results also showed that α-chaconine could inhibit phosphorylation of c-Jun N-terminal kinase (JNK) and Akt, whereas it did not affected phosphorylation of extracellular signal regulating kinase (ERK) and p38. In addition, α-chaconine significantly decreased the nuclear level of nuclear factor kappa B (NF-κB) and the binding ability of NF-κB. These results suggested that α-chaconine inhibited A549 cell metastasis by a reduction of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) activities involving suppression of phosphoinositide 3-kinase/Akt/NF-κB (PI3K/Akt/NF-κB) signaling pathway. Inhibiting metastasis by α-chaconine might offer a pivotal mechanism for its effective chemotherapeutic action.

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