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HS-173, a novel PI3K inhibitor suppresses EMT and metastasis in pancreatic cancer

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Title
HS-173, a novel PI3K inhibitor suppresses EMT and metastasis in pancreatic cancer
Author(s)
Rumman M.; Jung K.H.; Fang Z.; Yan H.H.; Son M.K.; Kim S.J.; Kim J.; Park J.H.; Lim J.H.; Sungwoo Hong; Hong S.-S.
Publication Date
2016-11
Journal
ONCOTARGET, v.7, no.47, pp.78029 - 78047
Publisher
IMPACT JOURNALS LLC
Abstract
Pancreatic cancer is one of the most aggressive solid malignancies prone to metastasis. Epithelial-mesenchymal transition (EMT) contributes to cancer invasiveness and drug resistance. In this study, we investigated whether HS-173, a novel PI3K inhibitor blocked the process of EMT in pancreatic cancer. HS-173 inhibited the growth of pancreatic cancer cells in a dose- and time-dependent manner. Moreover, it significantly suppressed the TGF-β-induced migration and invasion, as well as reversed TGF-β-induced mesenchymal cell morphology. Also, HS-173 reduced EMT by increasing epithelial markers and decreasing the mesenchymal markers by blocking the PI3K/AKT/mTOR and Smad2/3 signaling pathways in pancreatic cancer cells. In addition, HS-173 clearly suppressed tumor growth without drug toxicity in both xenograft and orthotopic mouse models. Furthermore, to explore the anti-metastatic effect of HS-173, we established pancreatic cancer metastatic mouse models and found that it significantly inhibited metastatic dissemination of the primary tumor to liver and lung. Taken together, our findings demonstrate that HS-173 can efficiently suppress EMT and metastasis by inhibiting PI3K/AKT/mTOR and Smad2/3 signaling pathways, suggesting it can be a potential candidate for the treatment of advanced stage pancreatic cancer
URI
http://pr.ibs.re.kr/handle/8788114/3258
DOI
10.18632/oncotarget.12871
ISSN
1949-2553
Appears in Collections:
Center for Catalytic Hydrocarbon Functionalizations(분자활성 촉매반응 연구단) > Journal Papers (저널논문)
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