Eupafolin suppresses prostate cancer by targeting phosphatidylinositol 3-kinase-mediated Akt signaling

Cited 17 time in scopus
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Title
Eupafolin suppresses prostate cancer by targeting phosphatidylinositol 3-kinase-mediated Akt signaling
Author(s)
K Liu; Chanmi Park; H Chen; Joonsung Hwang; N R Thimmegowda; Eun Young Bae; Ki Won Lee; H G Kim; H Liu; Nak Kyun Soung; C Peng; Jae-Hyuk Jang; K E Kim; Jong Seog Ahn; A M Bode; Z Dong; Kim Bo Yeon; Z Dong
Bibliographic Citation
Molecular Carcinogenesis, vol. 54, no. 9, pp. 751-760
Publication Year
2015
Abstract
Phosphatase and tensin homolog (PTEN) loss or mutation consistently activates the phosphatidylinositol 3-kinase (PI3-K)/Akt signaling pathway, which contributes to the progression and invasiveness of prostate cancer. Furthermore, the PTEN/PI3-K/Akt and Ras/MAPK pathways cooperate to promote the epithelial-mesenchymal transition (EMT) and metastasis initiated from prostate stem/progenitor cells. For these reasons, the PTEN/PI3-K/Akt pathway is considered as an attractive target for both chemoprevention and chemotherapy. Herein we report that eupafolin, a natural compound found in common sage, inhibited proliferation of prostate cancer cells. Protein content analysis indicated that phosphorylation of Akt and its downstream kinases was inhibited by eupafolin treatment. Pull-down assay and in vitro kinase assay results indicated that eupafolin could bind with PI3-K and attenuate its kinase activity. Eupafolin also exhibited tumor suppressive effects in vivo in an athymic nude mouse model. Overall, these results suggested that eupafolin exerts antitumor effects by targeting PI3-K.
Keyword
AktChemopreventionEupafolinPhosphatidylinositol 3-kinaseProstate cancer
ISSN
0899-1987
Publisher
Wiley
DOI
http://dx.doi.org/10.1002/mc.22139
Type
Article
Appears in Collections:
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
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