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2017 ; 14
(4
): 2895-2902
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Ginsenoside Rb1 inhibits hypoxia-induced epithelial-mesenchymal transition in
ovarian cancer cells by regulating microRNA-25
#MMPMID28928801
Liu D
; Liu T
; Teng Y
; Chen W
; Zhao L
; Li X
Exp Ther Med
2017[Oct]; 14
(4
): 2895-2902
PMID28928801
show ga
Metastasis frequently occurs in advanced ovarian cancer, which not only leads to
substantial mortality but also becomes a major challenge to effective treatment.
Epithelial-mesenchymal transition (EMT) is a key mechanism facilitating cancer
metastasis. Targeting the EMT process with more efficacious and less toxic agents
to prevent metastasis is of significant therapeutic value for ovarian cancer
treatment. The anti-EMT function and mechanism of ginsenoside Rb1, a monomer
composition extracted from the traditional Chinese herb Panax ginseng or P.
notoginseng, was investigated in the present study. Western blotting demonstrated
that treatment with ginsenoside Rb1 antagonized hypoxia-induced E-cadherin
downregulation and vimentin upregulation in SKOV3 and 3AO human ovarian cancer
cells. Wound healing assays and in vitro migration assays indicated that
ginsenoside Rb1 weakened hypoxia-enhanced cell migration ability. Furthermore, it
was demonstrated that microRNA (miR)-25 is upregulated by hypoxia in ovarian
cancer cells, which was attenuated by ginsenoside Rb1 treatment. Additionally,
forced expression of miR-25 in ovarian cancer cells was identified to not only
trigger EMT, but also block the suppressive effects of ginsenoside Rb1 on
hypoxia-induced EMT by negatively targeting the E-cadherin transactivator, EP300.
In conclusion, ginsenoside Rb1 may reverse hypoxia-induced EMT by abrogating the
suppression of miR-25 on EP300 and E-cadherin, which suggests that ginsenoside
Rb1 may be a potential therapeutic candidate for the treatment of ovarian cancer.
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