57326

PBXIP1

To date, hematopoietic pre-B cell leukemia transcription factor-interacting protein (HPIP), a co-repressor for the transcription factor PBX, has been involved into the initiation and onset in a wide variety of cancers. However, the molecular mechanisms underlying HPIP-induced epithelial-mesenchymal transition (EMT) in the spinal glioblastoma have been under investigation. In the present study, spinal glioblastoma tissues, U87, and U251 cell lines were used and subjected to in vitro assays, such as RT-PCR, and Western blot. Here, in vitro assays revealed that HPIP mRNA and protein were highly expressed in five cases of spinal glioblastoma tissues, compared with non-tumor tissues. Subsequently, in vitro experiments demonstrated HPIP promoted the U87 and U251 cell growth and regulated the G1/S phase transitions in U87 and U251 cell cycle, respectively, accompanied by the increased expression of cyclin A2, cyclin B1, and cyclin D1. Furthermore, HPIP increased the expression of N-cadherin, Slug, and MMP2, and decreased the expression of E-cadherin. By contrast, knockdown of HPIP reversed HPIP-induced EMT biomarkers, migration, and invasion in U87 and U251 cells. In conclusion, our findings identified HPIP plays an important role in the progression and EMT of spinal glioblastoma, by which cell growth is improved. Thus, HPIP gene or protein could act as a useful target in the clinical practice.

Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a nucleo-cytoplasmic 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)-beta1. In this study, we found that HPIP was highly expressed in ovarian cancer cells, and TGF-beta1 treatment induced HPIP expression in ovarian cancer cells. In addition, knockdown of HPIP suppressed TGF-beta1-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-beta1 in SKOV3 cells. In conclusion, the present study showed that HPIP silencing might prevent TGF-beta1-induced EMT in ovarian cancer cells. Thus, HPIP may be a potential therapeutic target for the treatment of ovarian cancer.