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HPIP Silencing Prevents Epithelial–Mesenchymal Transition Induced by TGF-β1 in Human Ovarian Cancer Cells

Guo-ying Zhang1, Ai-hua Liu1, Guo-min Li, Jian-rong Wang

Department of Obstetrics and Gynecology, Dongying People’s Hospital, Dongying, China
1 These authors provided equal contribution to this work.

Oncology Research 2016, 24(1), 33-39. https://doi.org/10.3727/096504016X14575597858654

Abstract

Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a nucleocytoplasmic shuttling protein, and its expression is associated with cancer aggressiveness. However, the role of HPIP in ovarian cancer is still unclear. Here, we aimed to clarify the role of HPIP in epithelial–mesenchymal transition (EMT) process of ovarian cancer cells, stimulated by transforming growth factor (TGF)-β1. In this study, we found that HPIP was highly expressed in ovarian cancer cells, and TGF-β1 treatment induced HPIP expression in ovarian cancer cells. In addition, knockdown of HPIP suppressed TGF-β1-induced EMT and migration/invasion in ovarian cancer cells. Moreover, knockdown of HPIP significantly blocked the phosphorylated pattern of both PI3K and Akt induced by TGF-β1 in SKOV3 cells. In conclusion, the present study showed that HPIP silencing might prevent TGF-β1-induced EMT in ovarian cancer cells. Thus, HPIP may be a potential therapeutic target for the treatment of ovarian cancer.

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APA Style
Zhang, G., Liu, A., Li, G., Wang, J. (2016). HPIP silencing prevents epithelial–mesenchymal transition induced by TGF-β1 in human ovarian cancer cells. Oncology Research, 24(1), 33-39. https://doi.org/10.3727/096504016X14575597858654
Vancouver Style
Zhang G, Liu A, Li G, Wang J. HPIP silencing prevents epithelial–mesenchymal transition induced by TGF-β1 in human ovarian cancer cells. Oncol Res. 2016;24(1):33-39 https://doi.org/10.3727/096504016X14575597858654
IEEE Style
G. Zhang, A. Liu, G. Li, and J. Wang, “HPIP Silencing Prevents Epithelial–Mesenchymal Transition Induced by TGF-β1 in Human Ovarian Cancer Cells,” Oncol. Res., vol. 24, no. 1, pp. 33-39, 2016. https://doi.org/10.3727/096504016X14575597858654



cc Copyright © 2016 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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