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Cypripedin diminishes an epithelial-to-mesenchymal transition in non-small cell
lung cancer cells through suppression of Akt/GSK-3? signalling
#MMPMID29789636
Treesuwan S
; Sritularak B
; Chanvorachote P
; Pongrakhananon V
Sci Rep
2018[May]; 8
(1
): 8009
PMID29789636
show ga
Lung cancer appears to have the highest rate of mortality among cancers due to
its metastasis capability. To achieve metastasis, cancer cells acquire the
ability to undergo a switch from epithelial to mesenchymal behaviour, termed the
epithelial-to-mesenchymal transition (EMT), which is associated with poor
clinical outcomes. Drug discovery attempts have been made to find potent
compounds that will suppress EMT. Cypripedin, a phenanthrenequinone isolated from
Thai orchid, Dendrobium densiflorum, exhibits diverse pharmacological activities.
In this study, we found that cypripedin attenuated typical mesenchymal
phenotypes, including migratory behaviour, of non-small cell lung cancer H460
cells, with a significant reduction of actin stress fibres and focal adhesion and
with weakened anchorage-independent growth. Western blot analysis revealed that
the negative activity of this compound on EMT was a result of the down-regulation
of the EMT markers Slug, N-Cadherin and Vimentin, which was due to ATP-dependent
tyrosine kinase (Akt) inactivation. As a consequence, the increase in the Slug
degradation rate via a ubiquitin-proteasomal mechanism was encouraged. The
observation in another lung cancer H23 cell line also supported this finding,
indicating that cypripedin exhibits a promising pharmacological action on lung
cancer metastasis that could provide scientific evidence for the further
development of this compound.
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