Isoaaptamine increases ROS levels causing autophagy and mitochondria-mediated apoptosis in glioblastoma multiforme cells

Wen, Zhi‐Hong; Kuo, Hsi-Kung; Shih, Po‐Chang; Hsu, Ling-Chen; Chuang, Jimmy Ming-Jung; Chen, Nan‐Fu; Sun, Hsi-Wen; Liu, Hsin-Tzu; Sung, Chun-Sung; Chen, Wu-Fu

doi:10.1016/j.biopha.2023.114359

Cited by 12 publications

(6 citation statements)

References 31 publications

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“…Isoaaptamine specifically induces ROS overproduction, up-regulates autophagy-associated proteins p62 and LC3, and forms acid organelle vesicles related to autophagy, leading to autophagic cell death (Wen et al. 2023 ). These findings underscore the potential of marine-derived compounds to induce autophagic cell death in glioma cells, highlighting their importance in cancer therapy.…”

Section: The Marine-derived Natural Products That Affect the Death Of...mentioning

confidence: 99%

Prospects of marine-derived compounds as potential therapeutic agents for glioma

Liu,

Zhou,

Sun

2024

Pharmaceutical Biology

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Section: The Marine-derived Natural Products That Affect the Death Of...mentioning

confidence: 99%

Prospects of marine-derived compounds as potential therapeutic agents for glioma

Liu,

Zhou,

Sun

2024

Pharmaceutical Biology

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“…Oxidative stress could regulate the apoptosis of glioma cells by Caspase pathway 12 , so we investigated the expression levels of caspase-7, Bcl-2 and Bax, which are associated with the apoptosis pathway. Western blot analysis was performed to measure protein levels of caspase-7, Bcl-2 and Bax in both circFOXO3-KD and NC cells.…”

Section: Bioinformatics Analysis Of Circfoxo3 and Associated Rna-bind...mentioning

confidence: 99%

CircFOXO3 Upregulation Mediates the Radioresistance of Glioblastoma by Affecting Cellular Metabolome

Xu,

Xing,

Cheng

et al. 2023

Preprint

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Radioresistance remains an important barrier to the treatment of glioblastoma multiforme (GBM), which is the most prevalent and lethal brain cancer in adults. Metabolic alterations contribute to radioresistance through various mechanisms, including activation of antioxidant responses to counteract reactive oxygen species (ROS) and DNA repair. In this study, we observed a significant up-regulation of circFOXO3 in glioma cells upon exposure to radiation and recurrent GBM tissues. Knockdown of circFOXO3 enhanced radiosensitivity in glioma cells. An assay of orthotopic GBM animal model in vivo indicated that inhibition of circFOXO3 significantly suppressed GBM progression and prolonged survival time. Overexpression of circFOXO3 significantly attenuated radiosensitivity in glioma cells. Additionally, metabolomics analysis revealed substantial alterations in the metabolomic profiles between the circFOXO3-OE and control groups following irradiation, particularly involving lipids and lipid-like molecules, organic acids and derivatives, and organoheterocyclic compounds. Moreover, suppression of circFOXO3 increased levels of pro-apoptotic proteins Caspase 7 and Bax while decreasing Bcl-2 levels after radiotherapy. Our findings establish the crucial role played by circFOXO3 in tumor radioresistance through modulation of metabolites, highlighting its potential as a diagnostic and therapeutic target for GBM.

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“…The activation of transient receptor potential mucolipin 1 (TRPML1) inhibits autophagy in glioma cells in vitro , leading to ROS production and subsequent induction of apoptosis ( 238 ). Similarly, the increase in ROS induced by isoaaptamine also leads to apoptosis and autophagy in GBM cells in vitro ( 26 ). Furthermore, the heat shock protein 90 (HSP90) and dynamin-related protein 1 (DRP1) increase ROS production by regulating the expression of acyl-coenzyme A synthetase long-chain family member 4 (ACSL4) and mitochondrial morphology, leading to ferroptosis of gliomas in mice in vitro and in vivo ( 239 ).…”

Section: The Role Of Ros In the Glioma Tmementioning

confidence: 99%

“…In gliomas, appropriate amounts of ROS can activate growth-related signalling pathways, induce DNA mutations, and promote invasion and metastasis ( 22 – 24 ). However, it has been shown that inducing ROS accumulation leads to glioma cell death ( 25 , 26 ). In contrast, given the critical role of ROS in the cell, the depletion of ROS also makes it difficult for glioma cells to survive ( 27 , 28 ).…”

Section: Introductionmentioning

confidence: 99%

ROS regulation in gliomas: implications for treatment strategies

Yang,

Zhu,

Sun

et al. 2023

Front. Immunol.

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Gliomas are one of the most common primary malignant tumours of the central nervous system (CNS), of which glioblastomas (GBMs) are the most common and destructive type. The glioma tumour microenvironment (TME) has unique characteristics, such as hypoxia, the blood-brain barrier (BBB), reactive oxygen species (ROS) and tumour neovascularization. Therefore, the traditional treatment effect is limited. As cellular oxidative metabolites, ROS not only promote the occurrence and development of gliomas but also affect immune cells in the immune microenvironment. In contrast, either too high or too low ROS levels are detrimental to the survival of glioma cells, which indicates the threshold of ROS. Therefore, an in-depth understanding of the mechanisms of ROS production and scavenging, the threshold of ROS, and the role of ROS in the glioma TME can provide new methods and strategies for glioma treatment. Current methods to increase ROS include photodynamic therapy (PDT), sonodynamic therapy (SDT), and chemodynamic therapy (CDT), etc., and methods to eliminate ROS include the ingestion of antioxidants. Increasing/scavenging ROS is potentially applicable treatment, and further studies will help to provide more effective strategies for glioma treatment.

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Isoaaptamine increases ROS levels causing autophagy and mitochondria-mediated apoptosis in glioblastoma multiforme cells

Cited by 12 publications

References 31 publications

Prospects of marine-derived compounds as potential therapeutic agents for glioma

Prospects of marine-derived compounds as potential therapeutic agents for glioma

CircFOXO3 Upregulation Mediates the Radioresistance of Glioblastoma by Affecting Cellular Metabolome

ROS regulation in gliomas: implications for treatment strategies

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