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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7273445 | PMC |
| http://dx.doi.org/10.1155/2020/8610271 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Radiofrequency Induced Time-Dependent Alterations in Gene Expression and Apoptosis in Glioblastoma Cell Line.
Bioelectromagnetics
January 2025
Department of Biophysics, Faculty of Medicine, Gazi University, Ankara, Turkey.
The widespread use of wireless communication technologies has increased human exposure to radiofrequency electromagnetic fields (RF-EMFs). Considering the brain's close proximity to mobile phones and its entirely electrical transmission network, it emerges as the organ most profoundly impacted by the RF field. This study aims to investigate the potential effects of RF radiation on cell viability, apoptosis, and gene expressions in glioblastoma cells (U118-MG) at different exposure times (1, 24, and 48 h).
View Article and Find Full Text PDFEngineered biomimetic cisplatin-polyphenol nanocomplex for chemo-immunotherapy of glioblastoma by inducing pyroptosis.
J Nanobiotechnology
January 2025
Department of Pharmacy The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Glioblastoma multiforme (GBM) is characterized by pronounced immune escape and resistance to chemotherapy-induced apoptosis. Preliminary investigations revealed a marked overexpression of gasdermin E (GSDME) in GBM. Notably, cisplatin (CDDP) demonstrated a capacity of inducing pyroptosis by activating caspase-3 to cleave GSDME, coupled with the release of proinflammatory factors, indicating the potential as a viable approach of inducing anti-tumor immune activation.
View Article and Find Full Text PDFIdentification of Key Biomarkers Associated with Glioma Hemorrhage: Evidence from Bioinformatic Analysis and Clinical Validation.
J Mol Neurosci
January 2025
Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.
Hemorrhagic stroke is a known complication of glioma, yet the underlying mechanisms remain poorly understood. This study aims to investigate key biomarkers of glioma-related hemorrhage to provide insights into glioma molecular therapies. Data were obtained from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) databases to analyze differentially expressed genes (DEGs) in glioma by contrasting glioblastoma (GBM) with low-grade gliomas (LGGs).
View Article and Find Full Text PDFFSD1 inhibits glioblastoma diffuse infiltration through restriction of HDAC6-mediated microtubule deacetylation.
Sci China Life Sci
January 2025
Nanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100850, China.
The infiltration of glioblastoma multiforme (GBM) is predominantly characterized by diffuse spread, contributing significantly to therapy resistance and recurrence of GBM. In this study, we reveal that microtubule deacetylation, mediated through the downregulation of fibronectin type III and SPRY domain-containing 1 (FSD1), plays a pivotal role in promoting GBM diffuse infiltration. FSD1 directly interacts with histone deacetylase 6 (HDAC6) at its second catalytic domain, thereby impeding its deacetylase activity on α-tubulin and preventing microtubule deacetylation and depolymerization.
View Article and Find Full Text PDFAdiponectin facilitates the cell cycle, inhibits cell apoptosis and induces temozolomide resistance in glioblastoma via the Akt/mTOR pathway.
Oncol Lett
March 2025
Department of Neurology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Adiponectin (ADN) regulates DNA synthesis, cell apoptosis and cell cycle to participate in the pathology and progression of glioblastoma. The present study aimed to further explore the effect of ADN on temozolomide (TMZ) resistance in glioblastoma and the underlying mechanism of action. Glioblastoma cell lines (U251 and U87-MG cells) were treated with ADN and TMZ at different concentrations; subsequently, 3.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!