HMGN5 Silencing Suppresses Cell Biological Progression via AKT/MAPK Pathway in Human Glioblastoma Cells.

Autor: Ma Q; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, China.; The Graduate School, Tianjin Medical University, Tianjin 300070, China., Wang X; Department of Neurosurgery, Tianjin First Center Hospital, Tianjin 300192, China., Wang H; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, China., Song W; The Graduate School, Tianjin Medical University, Tianjin 300070, China., Wang Q; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, China., Wang J; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin Neurosurgical Institute, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, China.
Jazyk: angličtina
Zdroj: BioMed research international [Biomed Res Int] 2020 May 21; Vol. 2020, pp. 8610271. Date of Electronic Publication: 2020 May 21 (Print Publication: 2020).
DOI: 10.1155/2020/8610271
Abstrakt: HMGN5 regulates biological function and molecular transcription via combining with a nucleosome. There has been growing evidence that aberrant expression of HMGN5 is associated with malignant neoplasm development and progression. In the present study, we found that the expression of HMGN5 is significantly higher in high-grade glioblastoma tissues than in low-grade samples. To clarify the function of HMGN5 in glioblastoma, we knocked down HMGN5 in U87 and U251 glioblastoma cells via siRNA. The results demonstrated that HMGN5 was involved in the regulation of proliferation and apoptosis, migration, and invasion of glioblastoma cells. These outcomes also indicated that silencing HMGN5 possibly suppressed the expression of p-AKT and p-ERK1/2. Taken together, our research reveals that HMGN5 might be an efficient target for glioblastoma-targeted therapy.
Competing Interests: All authors declare that they have no conflicts of interest.
(Copyright © 2020 Quanfeng Ma et al.)
Databáze: MEDLINE
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