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2018 ; 15
(4
): 4495-4502
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Casticin inhibits the epithelial-mesenchymal transition in ovarian carcinoma via
the hedgehog signaling pathway
#MMPMID29541219
Zhang J
; Cui Y
; Sun S
; Cao J
; Fang X
Oncol Lett
2018[Apr]; 15
(4
): 4495-4502
PMID29541219
show ga
Casticin inhibits migration, invasion and induced apoptosis in numerous cancer
cells; however, the Hedgehog (Hh) signaling pathway is a key factor in the
epithelial-mesenchymal transition (EMT). The present study aimed to assess
whether casticin affects the expression of members of the Hh signaling pathway
and EMT effectors in ovarian carcinoma. The ovarian cancer SKOV3 cell line was
incubated in the presence of various concentrations of casticin or cyclopamine.
Next, the expression levels of the main Hh signaling effector glioma-associated
oncogene-1 (Gli-1) and EMT-associated factors [Twist-related protein 1 (Twist1),
E-cadherin and N-cadherin] were determined by western blotting and reverse
transcription-quantitative polymerase chain reaction. Cell proliferation and
growth were assessed using MTT and soft agar assays; cell migration and invasion
was evaluated using an in vitro migration assay and a transwell invasion assay,
respectively. Compared with control group values, Gli-1, Twist1 and N-cadherin
expression levels were reduced, whereas E-cadherin levels were increased in the
casticin- and cyclopamine-treated groups. Incubation with casticin or cyclopamine
resulted in markedly reduced SKOV3 cell viability, migration and invasion, in a
dose-dependent manner. To the best of our knowledge, the findings of the present
study indicated for first time that casticin may inhibit EMT via Hh signaling in
vitro, reducing the migratory ability of ovarian cancer cells.