Glioblastoma is a highly malignant cancer of glioma cells. Present study investigates the anti proliferative activity of granatin B on glioma cell by inducing apoptosis. In this study Glioma cell (U87) was used on which anti proliferative activity of granatin B (0, 20, 40 & 80 µM) assessed by 3-(4, 5-dimethylthylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay. Thereafter Apoptosis of glioma cell was assessed by apoptosis detection kit suing flow cytometer, DAPI staining and by estimating the activity of caspase 3 & 9 using caspase 3 & 9 kit. Expression of MMP9 protein was determined through gelatin zymography. Possible mechanism of apoptosis induction was proved by estimating the effect of granatin B with MMP9 agonist on cell proliferation, caspase 3 activity & MMP9 expression on glioblastoma cell. Result of the study suggested that granatin B significantly decreases the cell proliferation of glioma cell compared to 0 µM treated group. It was also observed that treatment with granatin B significantly induces apoptosis and increases the activity of caspase 3 & 9 protein compared to 0 µM treated group. Expression of MMP9 protein was also decreases with granatin B treatment of glima cell. MMP9 agonist significantly reverses the effect of granatin B on cell proliferation, caspase 3 and expression of MMP9 protein in glima cell. Present study concludes the anticancer activity of granatin B on glioblastoma cell by inducing apoptosis.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040695 | PMC |
Publication Analysis
Top Keywords
Similar Publications
The phosphodiesterase-4 inhibitor Zl-n-91 suppresses glioblastoma growth via EGR1/PTEN/AKT pathway.
Eur J Pharmacol
December 2024
The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, PR China. Electronic address:
Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor, which presents significant challenges for treatment in clinical settings. Phosphodiesterase 4 (PDE4) inhibitors can prevent the degradation of cAMP and have been used as a potential targeted therapeutic approach for different cancer types. However, its clinical use is restricted by the side effects such as nausea and vomiting.
View Article and Find Full Text PDFPTEN loss in glioma cell lines leads to increased extracellular vesicle biogenesis and PD-L1 cargo in a PI3K-dependent manner.
J Biol Chem
December 2024
Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA; Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, 14853, USA. Electronic address:
Phosphatase and Tensin Homologue (PTEN) is one of the most frequently lost tumor suppressors in cancer and the predominant negative regulator of the PI3K/AKT signaling axis. A growing body of evidence has highlighted the loss of PTEN with immuno-modulatory functions including the upregulation of the programmed death ligand-1 (PD-L1), an altered tumor derived secretome that drives an immunosuppressive tumor immune microenvironment (TIME), and resistance to certain immunotherapies. Given their roles in immunosuppression and tumor growth, we examined whether the loss of PTEN would impact the biogenesis, cargo, and function of extracellular vesicles (EVs) in the context of the anti-tumor associated cytokine interferon-γ (IFN-γ).
View Article and Find Full Text PDFExosomes as nature's nano carriers: Promising drug delivery tools and targeted therapy for glioma.
Biomed Pharmacother
December 2024
Department of Biotechnology and Research, Sir Ganga Ram Hospital, New Delhi 110060, India.
Exosomes, minute vesicles originating from diverse cell types, exhibit considerable potential as carriers for drug delivery in glioma therapy. These naturally occurring nanocarriers facilitate the transfer of proteins, RNAs, and lipids between cells, offering advantages such as biocompatibility, efficient cellular absorption, and the capability to traverse the blood-brain barrier (BBB). In the realm of cancer, particularly gliomas, exosomes play pivotal roles in modulating tumor growth, regulating immunity, and combating drug resistance.
View Article and Find Full Text PDFAutophagy Modulates Glioblastoma Cell Sensitivity to Selinexor-mediated XPO1 inhibition.
Neuro Oncol
December 2024
Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Selinexor is a selective inhibitor of exportin-1 (XPO1), a key mediator of the nucleocytoplasmic transport for molecules critical to tumor cell survival. Selinexor's lethality is generally associated with the induction of apoptosis, and in some cases, with autophagy-induced apoptosis. We performed this study to determine Selinexor's action in glioblastoma (GBM) cells, which are notoriously resistant to apoptosis.
View Article and Find Full Text PDFCopper-coordination driven brain-targeting nanoassembly for efficient glioblastoma multiforme immunotherapy by cuproptosis-mediated tumor immune microenvironment reprogramming.
J Nanobiotechnology
December 2024
Key Laboratory of Emergency and Trauma of Ministry of Education, Engineering Research Center for Hainan Biological Sample Resources of Major Diseases, the Hainan Branch of National Clinical Research Center for Cancer, the First Affiliated Hospital, Hainan Medical University, Haikou, 570102, China.
Limited drug accumulation and an immunosuppressive microenvironment are the major bottlenecks in the treatment of glioblastoma multiforme (GBM). Herein, we report a copper-coordination driven brain-targeting nanoassembly (TCe6@Cu/TP5 NPs) for site-specific delivery of therapeutic agents and efficient immunotherapy by activating the cGAS-STING pathway and downregulating the expression of PD-L1. To achieve this, the mitochondria-targeting triphenylphosphorus (TPP) was linked to photosensitizer Chlorin e6 (Ce6) to form TPP-Ce6 (TCe6), which was then self-assembled with copper ions and thymopentin (TP5) to obtain TCe6@Cu/TP5 NPs.
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!