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Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation.

ABSTRACT: Glioblastoma (GBM) is the most common type of primary brain tumor. Patients with GBM have poor survival outcomes. Isolated components of Momordica charantia have anticancer effects. However, the bioactivity of M. charantia extracts against GBM remains unknown. We tested four major extracts of M. charantia and found that momordicine I reduced glioma cell viability without serious cytotoxic effects on astrocytes. Momordicine I suppressed glioma cell colony formation, proliferation, migration, and invasion. Momordicine I also induced apoptosis, intracellular reactive oxygen species (ROS) production, and senescence in glioma cells. Moreover, momordicine I decreased the oxidative phosphorylation capacity of glioma cells and inhibited tumor sphere formation in temozolomide (TMZ)-resistant GBM cells. We further explored whether the antiglioma effect of momordicine I may be related to cell cycle modulation and DLGPA5 expression. Our results indicate that the cytotoxic effect of momordicine I on glioma cells suggests its potential therapeutic application to GBM treatment. See also Figure 1(Fig. 1).

SUBMITTER: Kao Y

PROVIDER: S-EPMC10391611 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation.

Kao Ying Y Chou Chung-Hsing CH Huang Li-Chun LC Tsai Chia-Kuang CK

EXCLI journal 20230606

Glioblastoma (GBM) is the most common type of primary brain tumor. Patients with GBM have poor survival outcomes. Isolated components of Momordica charantia have anticancer effects. However, the bioactivity of M. charantia extracts against GBM remains unknown. We tested four major extracts of M. charantia and found that momordicine I reduced glioma cell viability without serious cytotoxic effects on astrocytes. Momordicine I suppressed glioma cell colony formation, prolifera ...[more]

PMID: 37534227

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Project description:Globally, prostate cancer is among the most threatening and leading causes of death in men. This study, therefore, aimed to search for an ideal antitumor strategy with high efficacy, low drug resistance, and no or few adverse effects. Resistomycin is a natural antibiotic derived from marine actinomycetes, and it possesses various biological activities. Prostate cancer cells (PC3) were treated with resistomycin (IC12.5: 0.65 or IC25: 1.3 µg/mL) or 5-fluorouracil (5-FU; IC25: 7 µg/mL) for 24 h. MTT assay and flow cytometry were utilized to assess cell viability and apoptosis. Oxidative stress, apoptotic-related markers, and cell cycle were also assessed. The results revealed that the IC50 of resistomycin and 5-FU on PC3 cells were 2.63 µg/mL and 14.44 µg/mL, respectively. Furthermore, treated cells with the high dose of resistomycin showed an increased number of apoptotic cells compared to those treated with the lower dose. Remarkable induction of reactive oxygen species generation and lactate dehydrogenase (LDH) leakage with high malondialdehyde (MDA), carbonyl protein (CP), and 8-hydroxyguanosine (8-OHdG) contents were observed in resistomycin-treated cells. In addition, marked declines in glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in PC3 cells subjected to resistomycin therapy were observed. Resistomycin triggered observable cell apoptosis by increasing Bax, caspase-3, and cytosolic cytochrome c levels and decreasing Bcl-2 levels. In addition, notable downregulation of proliferating cell nuclear antigen (PCNA) and cyclin D1 was observed in resistomycin-treated cancerous cells. According to this evaluation, the antitumor potential of resistomycin, in a concentration-dependent manner, in prostate cancer cells was achieved by triggering oxidative stress, mitochondrial apoptosis, and cell cycle arrest in cancer cells. In conclusion, our investigation suggests that resistomycin can be considered a starting point for developing new chemotherapeutic agents for human prostate cancer.

Dataset Information

Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation.

Publications

Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation.

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