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HPIP Silencing Prevents Epithelial-Mesenchymal Transition Induced by TGF-beta 1 in Human Ovarian Cancer Cells

机译:HPIP沉默防止人类卵巢癌细胞中TGF-beta 1诱导的上皮-间质转化。

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摘要

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)-beta 1. In this study, we found that HPIP was highly expressed in ovarian cancer cells, and TGF-beta 1 treatment induced HPIP expression in ovarian cancer cells. In addition, knockdown of HPIP suppressed TGF-beta 1-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-beta 1 in SKOV3 cells. In conclusion, the present study showed that HPIP silencing might prevent TGF-beta 1-induced EMT in ovarian cancer cells. Thus, HPIP may be a potential therapeutic target for the treatment of ovarian cancer.
机译:造血前B细胞白血病转录因子(PBX)相互作用蛋白(HPIP / PBXIP1)是一种核质穿梭蛋白,其表达与癌症侵袭性相关。但是,HPIP在卵巢癌中的作用仍不清楚。在这里,我们旨在阐明HPIP在转化生长因子(TGF)-beta 1刺激下在卵巢癌细胞上皮-间质转化(EMT)过程中的作用。在这项研究中,我们发现HPIP在卵巢癌中高表达。 TGF-beta 1处理可诱导卵巢癌细胞HPIP表达。此外,敲低HPIP抑制了TGF-β1诱导的EMT和卵巢癌细胞的迁移/侵袭。而且,HPIP的敲低显着阻断了SKOV3细胞中TGF-beta 1诱导的PI3K和Akt的磷酸化模式。总之,本研究表明HPIP沉默可能阻止TGF-β1诱导的卵巢癌细胞EMT。因此,HPIP可能是治疗卵巢癌的潜在治疗靶标。

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