TY - JOUR
T1 - Inhibition of migration and invasion in melanoma cells by β-escin via the ERK/NF-κB signaling pathway
AU - Kwak, Hyeong Seob
AU - An, Hongyan
AU - Alam, Md Badrul
AU - Choi, Won Sik
AU - Lee, Sang
AU - Lee, Sang Han
N1 - Publisher Copyright:
© 2018 The Pharmaceutical Society of Japan
PY - 2018
Y1 - 2018
N2 - β-Escin, a natural triterpene saponin was extracted from Aesculus hippocastanum seeds, which have been widely used to treat inflammation in traditional medicine. In an effort to study the possible anti-tumor effects of β-escin, we performed wound healing, invasion, and adhesion assays to examine the effects of β-escin on cell migration, invasion, and angiogenesis. Our results revealed that β-escin inhibits cell migration as well as motility in B16F10 and SK-MEL5 cells in a dose-dependent manner. RT-PCR and Western blot analysis showed that β-escin increased TIMP-1, -2 while significantly downregulated phosphorylated extracellular signal-regulated kinase (p-ERK) expression, and suppressing nuclear factor-kappa B (NF-κB) and inhibitor of nuclear factor-kappa B (IκB) expression. Overall, the data from the current study suggest that β-escin has the potential for inhibiting both metastatic and angiogenic activities, and are the earliest evidence for the involvement of the NF-κB/IκB signaling in β-escin-induced anti-tumor effects.
AB - β-Escin, a natural triterpene saponin was extracted from Aesculus hippocastanum seeds, which have been widely used to treat inflammation in traditional medicine. In an effort to study the possible anti-tumor effects of β-escin, we performed wound healing, invasion, and adhesion assays to examine the effects of β-escin on cell migration, invasion, and angiogenesis. Our results revealed that β-escin inhibits cell migration as well as motility in B16F10 and SK-MEL5 cells in a dose-dependent manner. RT-PCR and Western blot analysis showed that β-escin increased TIMP-1, -2 while significantly downregulated phosphorylated extracellular signal-regulated kinase (p-ERK) expression, and suppressing nuclear factor-kappa B (NF-κB) and inhibitor of nuclear factor-kappa B (IκB) expression. Overall, the data from the current study suggest that β-escin has the potential for inhibiting both metastatic and angiogenic activities, and are the earliest evidence for the involvement of the NF-κB/IκB signaling in β-escin-induced anti-tumor effects.
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U2 - 10.1248/bpb.b18-00251
DO - 10.1248/bpb.b18-00251
M3 - Article
C2 - 30270331
AN - SCOPUS:85054250995
SN - 0918-6158
VL - 41
SP - 1606
EP - 1610
JO - Biological and Pharmaceutical Bulletin
JF - Biological and Pharmaceutical Bulletin
IS - 10
ER -