Alterations in the expression of microRNA (miR)‑138 have been demonstrated to result in the development of several malignant tumours. However, the possible function of miR‑138 in human glioma cells remains unclear. The present study demonstrated that miR‑138 was significantly downregulated in 48 human glioma specimens by quantitative PCR analysis. The upregulation of miR‑138 exerted significant antiproliferative and anti‑invasive effects on glioma cells and promoted their apoptosis. In addition, cAMP response element‑binding protein 1 (CREB1) was confirmed as a direct target gene of miR‑138 by luciferase gene reporter assay, and the antitumour effect of miR‑138 on glioma cells was significantly reversed by CREB1 overexpression. Moreover, the molecular mechanisms underlying the tumour‑suppressive role of miR‑138 in malignant glioma may be associated with the dephosphorylation of AKT/mTOR caused by the miR‑138 upregulation‑induced decrease in CREB1 expression in glioma cells. The results of the present study indicated that miR‑138 may affect CREB1/AKT/mTOR signalling to regulate the proliferation, apoptosis and invasion of glioma cells and the malignant progression of glioma, thereby suggesting that miR‑138 may be a potential target for the treatment of gliomas.
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http://dx.doi.org/10.3892/or.2020.7809 | DOI Listing |
Chembiochem
January 2025
Xidian University, School of Life Science and Technology, 266 Xinglong Section of Xifeng Road, 710126, Xi'an, CHINA.
The resistance of cancer cells to apoptosis poses a significant challenge in cancer therapy, driving the exploration of alternative cell death pathways such as pyroptosis, known for its rapid and potent effects. While initial efforts focused on chemotherapy-induced pyroptosis, concerns about systemic inflammation highlight the need for precise activation strategies. Photothermal therapy emerges as a promising non-invasive technique, minimizing pyroptosis-related side effects by targeting tumors spatially and temporally.
View Article and Find Full Text PDFAdv Healthc Mater
January 2025
School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200240, P. R. China.
Modern radiotherapy frequently employs radiosensitizers for radiation dose deposition and triggers an immunomodulatory effect to enhance tumor destruction. However, developing glioma-targeted sensitizers remains challenging due to the blood-brain barrier (BBB) and multicomponent instability. This study aims to green-synthesize transferrin-bismuth nanoparticles (TBNPs) as biosafe radiosensitizers to enhance X-ray absorption by tumors and stimulate the immune response for glioma therapy.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Departamento de Biología Molecular y Bioquímica, Universidad de Málaga, 29071 Málaga, Spain.
Glutaminase controls the first step in glutaminolysis, impacting bioenergetics, biosynthesis and oxidative stress. Two isoenzymes exist in humans, GLS and GLS2. GLS is considered prooncogenic and overexpressed in many tumours, while GLS2 may act as prooncogenic or as a tumour suppressor.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Biological, Geological and Environmental Sciences, University of Bologna, Via Selmi 3, 40126 Bologna, Italy.
This study aimed to investigate β-Caryophyllene (BCA) pharmacokinetics as well as the potential antitumor activity and mechanism of action of BCA and eugenol (EU), alone or in combination, in U87 glioblastoma (GB) cells. The BCA pharmacokinetic was studied by evaluating its concentration profiles in rat blood and cerebrospinal fluid after oral and intravenous administration. EU and BCA antitumor mechanisms were assessed by comparing their effects in U87 GB cells and non-tumoral HMC3 cells.
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