Dataset Information

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

ABSTRACT: 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.

SUBMITTER: Ma Q

PROVIDER: S-EPMC7273445 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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

Ma Quanfeng Q Wang Xiuyu X Wang Hong H Song Wen W Wang Qiong Q Wang Jinhuan J

BioMed research international 20200521

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 re ...[more]

PMID: 32596388

Similar Datasets

Project description:BackgroundEsophageal cancer is the sixth leading cause of cancer-related mortality worldwide, which is partially due to limited progress of therapy. Apatinib, an inhibitor of VEGFR2, has a promising antitumor effect on malignancies. However, the underlying mechanism of its antitumor effect on esophageal cancer remains poorly understood.Materials and methodsEighteen pairs of frozen esophageal cancer and their para-cancer samples and 25 paraffin specimens from advanced esophageal cancer patients treated with cisplatin-based regimen were collected. The effects of apatinib on cell growth, cell apoptosis, cell cycle and invasion/migration of esophageal cancer cells were assessed. Bioinformatics, luciferase reporter, immunoprecipitation and immunofluorescence assays were conducted for mechanic investigation. Quantitative RT-PCR, western blotting and immunohistochemistry were used to measure the expression of functional genes. Xenograft tumor growth of mice was performed.ResultsWe found that VEGFR2 was highly expressed in esophageal cancer and associated with poor efficacy of cisplatin-based treatment. Apatinib displayed profound actions against tumor cell growth of human esophageal cancer via promoting cell apoptosis and cell cycle arrest. Also, apatinib displayed the inhibitory effects on cell migration and invasion. Moreover, apatinib strongly suppressed the growth of esophageal cancer xenografts in mice. The effects of apatinib on esophageal cancer were partially dependent on its block of the VEGFR2/Akt/?-catenin pathway. Specifically, apatinib induced the degradation of ?-catenin and decreased its transcriptional activity through Akt/GSK-3? repression. Further in vitro and in vivo studies revealed that low dose apatinib had a synergistic antitumor effect with cisplatin on esophageal cancer.ConclusionOur study indicates that apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer by deactivating the Akt/?-catenin pathway. These findings provide a theoretical foundation for using apatinib as an effective therapeutic drug for esophageal cancer.

Project description:Background:Retroperitoneal liposarcoma (RLPS) is a rare tumor with high recurrence rate. Ribonucleotide reductase small subunit M2 (RRM2) protein is essential for DNA synthesis and replication. Our previous study has demonstrated that RRM2 downregulation inhibited the proliferation of RLPS cells, but further association between RRM2 and RLPS and relevant mechanisms remains to be explored. Methods:RRM2 expression was evaluated in RLPS tumor tissues and cell lines by using real-time PCR and immunohistochemical analysis. The effect of RRM2 downregulation on cell proliferation, apoptosis, cell cycle, cell migration and invasion was tested by lentivirus. The effect of RRM2 inhibition on tumor growth in vivo was assessed by using patient-derived tumor xenograft (PDX) of RLPS and RRM2 inhibitor. The underlying mechanisms of RRM2 in RLPS were explored by protein microarray and Western blotting. Results:The results showed that RRM2 mRNA expression was higher in RLPS tissues than in normal fatty tissues (P<0.001). RRM2 expression was higher in the dedifferentiated, myxoid/round cell, and pleomorphic subtypes (P=0.027), and it was also higher in the high-grade RLPS tissues compared to that in the low-grade RLPS tissues (P=0.004). There was no correlation between RRM2 expression and overall survival (OS) or disease-free survival (DFS) in this group of RLPS patients (P>0.05). RRM2 downregulation inhibited cell proliferation, promoted cell apoptosis, facilitated cell cycle from G1 phase to S phase and inhibited cell migration and invasion. Inhibition of RRM2 suppressed tumor growth in NOD/SCID mice. Protein microarray and Western blot verification showed that activity of Akt/mammalian target of rapamycin/eukaryotic translation initiation factor 4E binding protein 1 (Akt/mTOR/4EBP1) pathway was downregulated along with RRM2 downregulation. Conclusion:RRM2 was overexpressed in RLPS tissues, and downregulation of RRM2 could inhibit RLPS progression. In addition, suppression of RRM2 is expected to be a promising treatment for RLPS patients.

Dataset Information

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

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets