Epithelial-mesenchymal transition (EMT) has been reported to play an important role in the migration and invasion of tumor cells. Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) has emerged as an important regulator… Click to show full abstract
Epithelial-mesenchymal transition (EMT) has been reported to play an important role in the migration and invasion of tumor cells. Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) has emerged as an important regulator of the development of cancer. However, the role of HPIP in lung cancer is unclear. Thus, in the present study, we investigated the role of HPIP in transforming growth factor (TGF)-β1-induced EMT in A549 lung cancer cells in vitro. Our data demonstrated that HPIP was overexpressed in the lung cancer cell lines. TGF-β1 increased the expression of HPIP in the A549 cells. In addition, HPIP silencing significantly attenuated TGF-β1-induced EMT and migration/invasion in the A549 cells. Furthermore, knockdown of HPIP greatly inhibited TGF-β1-induced phosphorylation of Smad2 in the A549 cells. In conclusion, we demonstrated that HPIP silencing suppressed TGF-β1-induced EMT in lung cancer cells by inhibiting Smad2 activation. Therefore, HPIP may be a new therapeutic target for the treatment of lung cancer.
               
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