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Recent studies revealed an antioxidant activity and anticancer efficiency of betanin. In this study, we investigated the cytotoxic effects and the possible mechanisms of betanin-induced apoptosis against U87MG human glioma cells and compared the results to those of human normal lymphocytes. MTT assay, caspase-3 activation assays in cells and succinate dehydrogenases (SDH), mitochondrial swelling, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), and cytochrome C release assays in isolated mitochondria were obtained from U87MG human glioma cells and noncancerous human lymphocytes The results illustrated the significant cytotoxic effect of betanin on U87MG human glioma cells, with a concentration value that inhibits 50% of the cell growth of 7 µg/ml after 12 h of treatment. MTT assay demonstrated that the betanin is selectively toxic to U87MG human glioma cells, and betanin induced cell apoptosis via activation of caspase-3 along with modulation of apoptosis-related mitochondria. Meanwhile, betanin selectively increased ROS formation, mitochondria swelling, MMP decrease, and cytochrome c release in cancerous mitochondria but in normal mitochondria. Based on the evidence obtained from this study, it is concluded that the betanin is a promising natural compound to fight U87MG human glioma cells via induction of apoptosis through activation of intrinsic pathways.
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http://dx.doi.org/10.1080/01635581.2020.1764068 | DOI Listing |
Mol Biol Rep
September 2025
Dr. B. R. Ambedkar Centre for Biomedical Research North Campus , University of Delhi, 110007, Delhi, India.
Background: Standard treatment for glioblastoma includes chemotherapy, alkylating agents such as temozolomide (TMZ); however, MGMT resistance leads to recurrence. Demethoxycurcumin (DMC) has been reported to inhibit cancer cell growth, induce apoptosis, and prevent metastasis in different cancer models. We investigated the DMC-induced apoptosis and autophagy via inhibition of the AKT/mTOR pathway in human glioma U87MG and T98G cell lines.
View Article and Find Full Text PDFCell Mol Biol Lett
September 2025
Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India.
Background: Autophagy, a conserved intracellular degradation process, plays dual roles in cancer, promoting survival under stress or mediating cell death through deregulated autophagy. Atypical cadherin FAT1 functions as an oncogene or tumor suppressor in a context-dependent manner. Our previous work identifies the oncogenic role of FAT1 in glioblastoma.
View Article and Find Full Text PDFJ Physiol
September 2025
Department of Chemistry, Biology, and Biotechnology, University of Perugia, Perugia, Italy.
Cell volume regulation is a complex homeostatic process employed by nearly all cell types to adapt to osmotic perturbations and to support physiological processes such as proliferation and migration. This process is critically dependent on the activity of ion channels and transporters, which modulate intracellular water content through the controlled movement of osmolytes across the plasma membrane. We recently demonstrated in a human glioblastoma (GBM) cell line (U87-MG) that hypotonic-induced Ca influx through mechanosensitive channels is crucial for activating both large- (BK) and intermediate- (IK) conductance Ca-activated K⁺ (K) channels, which in turn drive the regulatory volume decrease (RVD) response.
View Article and Find Full Text PDFEndoplasmic reticulum stress and glucose supply are significant factors in glioblastoma growth. The present study aims to investigate the impact of glucose-dependent control of , , , , , and gene expression in U87MG glioblastoma cells in response to the inhibition of both enzymatic activities of signaling protein ERN1. The U87MG glioblastoma cells with inhibited both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used.
View Article and Find Full Text PDFAnticancer Res
September 2025
School of Medicine, I-Shou University, Kaohsiung, Taiwan, R.O.C.
Background/aim: Glioblastoma (GBM) is a highly aggressive brain tumor associated with poor prognosis and frequent resistance to standard treatments, including temozolomide (TMZ) and radiotherapy. Our previous study identified superoxide dismutase 2 (SOD2) as a key contributor to TMZ resistance through enhanced antioxidant defenses. This study aimed to determine whether SOD2 also plays a role in reduced radiation sensitivity in TMZ-resistant GBM cells.
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