ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
The involvement of hematopoietic pre-B cell leukemia transcription factor-interacting protein in regulating epithelial-mesenchymal transition of human spinal glioblastoma.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Golgiphagy: a novel selective autophagy to the fore.Cell & bioscience · 2024Review
- Hematopoietic PBX-interacting protein is a substrate and an inhibitor of the APC/C-Cdc20 complex and regulates mitosis by stabilizing cyclin B1.The Journal of biological chemistry · 2019Article
- Hematopoietic PBX-interacting protein mediates cartilage degeneration during the pathogenesis of osteoarthritis.Nature communications · 2019Article
- HPIP: a predictor of lymph node metastasis and poor survival in cervical cancer.OncoTargets and therapy · 2017Article
- Expression of HPIP in epithelial ovarian carcinoma: a clinicopathological study.OncoTargets and therapy · 2017Article
- MicroRNA-520b affects the proliferation of human glioblastoma cells by directly targeting cyclin D1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- HPIP Silencing Prevents Epithelial-Mesenchymal Transition Induced by TGF-β1 in Human Ovarian Cancer Cells.Oncology research · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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