Targeting X box-binding protein-1 (XBP1) enhances sensitivity of glioma cells to oxidative stress

Liu, Y.; Zhang, X.; Yuan, Liang; Yu, Haoyang; Chen, X.; Zheng, Tianyue; Zheng, Bing; Wang, L.; Zhao, Lei; Shi, Changhong; Zhao, Shen

doi:10.1111/j.1365-2990.2010.01155.x

Cited by 28 publications

(20 citation statements)

References 37 publications

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“…Human glioma cell lines, U87MG and T98G were cultured in DMEM(Hyclone, Logan, UT, USA) supplemented with 10% FBS(Hyclone, Logan, UT, USA) at 37°C in a humidified CO 2 incubator, and 1% penicillin-streptomycin. The cells were passaged twice weekly, and once they were nearly confluent, they were released with 0.25% trypsin-ethylenediaminetetraacetic acid (EDTA) [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas

et al. 2014

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BackgroundAmong glioma treatment strategies, arsenic trioxide (As2O3) has shown efficacy as a therapeutic agent against human gliomas. However, the exact antitumor mechanism of action of As2O3 is still unclear. Mitochondria are considered to be the major source of intracellular reactive oxygen species (ROS), which are known to be associated with As2O3-induced cell damage. Therefore, we investigated whether mitoferrin-2, a mitochondrial iron uptake transporter, participates in As2O3-induced cell killing in human gliomas.MethodsHuman glioma cell lines were used to explore the mechanism of As2O3’s antitumor effects. First, expression of mitoferrin-2 was analyzed in glioma cells that were pretreated with As2O3. Changes in ROS production and apoptosis were assessed. Furthermore, cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT).ResultsIn the present study we found that As2O3 induced ROS production and apoptosis in glioma cells. In addition, gene expression of mitoferrin-2, a mitochondrial iron uptake transporter, was increased 4 to 5 fold after exposure to As2O3 (5 μM) for 48 hours. Furthermore, apoptosis and cytotoxicity induced by As2O3 in glioma cells were decreased after silencing the mitoferrin-2 gene.ConclusionsOur findings indicated that mitoferrin-2 participates in mitochondrial ROS-dependent mechanisms underlying As2O3-mediated damage in glioma cells.

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Section: Methodsmentioning

confidence: 99%

The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas

et al. 2014

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“…These results provide evidences that deactivation of the IRE1α-XBP1 [ 46 ] could be a target of anticancer therapy. For instance, IRE1α inhibitor rendered resistant human glioblastoma cells susceptible to oxidative stress [ 47 ]. Inhibition of IRE1α decreased endonuclease activity, increasing cytotoxic activity against human multiple myeloma in vitro and in vivo [ 48 ].…”

Section: Anti-cancer Strategy Based On Adaptive Pathway Of Er Strementioning

confidence: 99%

Anti-Cancer Natural Products and Their Bioactive Compounds Inducing ER Stress-Mediated Apoptosis: A Review

2018

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Cancer is the second biggest cause of death worldwide. Despite a number of studies being conducted, the effective mechanism for treating cancer has not yet been fully understood. The tumor-microenvironment such as hypoxia, low nutrients could disturb function of endoplasmic reticulum (ER) to maintain cellular homeostasis, ultimately leading to the accumulation of unfolded proteins in ER, so-called ER stress. The ER stress has a close relation with cancer. ER stress initiates unfolded protein response (UPR) to re-establish ER homeostasis as an adaptive pathway in cancer. However, persistent ER stress triggers the apoptotic pathway. Therefore, blocking the adaptive pathway of ER stress or facilitating the apoptotic pathway could be an anti-cancer strategy. Recently, natural products and their derivatives have been reported to have anti-cancer effects via ER stress. Here, we address mechanisms of ER stress-mediated apoptosis and highlight strategies for cancer therapy by utilizing ER stress. Furthermore, we summarize anti-cancer activity of the natural products via ER stress in six major types of cancers globally (lung, breast, colorectal, gastric, prostate and liver cancer). This review deepens the understanding of ER stress mechanisms in major cancers as well as the suppressive impact of natural products against cancers via ER stress.

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“…Under these conditions oxidative stress is a common factor providing extensive opportunities for ER-mitochondrial crosstalk, as both organelles participate in maintaining, initiating and responding to changes in redox state [110, 111]. For example, the UPR is engaged upon oxidative stress and is necessary to prevent and protect against mitochondrial dysfunction [112, 113]. One avenue through which this occurs is through the Ire1/Xbp1 pathway increasing expression of antioxidant machinery, such as catalase, thus preserving mitochondrial function.…”

Section: Pathophysiological Implications Of the Er-mitochondria Inmentioning

confidence: 99%

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Bravo-Sagua¹,

Rodríguez²,

Kuzmicic³

et al. 2013

Current Molecular Medicine

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The endoplasmic reticulum has a central role in biosynthesis of a variety of proteins and lipids. Mitochondria generate ATP, synthesize and process numerous metabolites, and are key regulators of cell death. The architectures of endoplasmic reticulum and mitochondria change continually via the process of membrane fusion, fission, elongation, degradation, and renewal. These structural changes correlate with important changes in organellar function. Both organelles are capable of moving along the cytoskeleton, thus changing their cellular distribution. Numerous studies have demonstrated coordination and communication between mitochondria and endoplasmic reticulum. A focal point for these interactions is a zone of close contact between them known as the mitochondrial–associated endoplasmic reticulum membrane (MAM), which serves as a signaling juncture that facilitates calcium and lipid transfer between organelles. Here we review the emerging data on how communication between endoplasmic reticulum and mitochondria can modulate organelle function and determine cellular fate.

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Targeting X box-binding protein-1 (XBP1) enhances sensitivity of glioma cells to oxidative stress

Abstract: XBP1 confers an important role in protection against oxidative stress in gliomas, potentially via up-regulation of antioxidant molecules such as catalase. Targeting XBP1 may have synergistic effects with ROS inducers on glioma treatment.

Cited by 28 publications

References 37 publications

The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas

The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas

Anti-Cancer Natural Products and Their Bioactive Compounds Inducing ER Stress-Mediated Apoptosis: A Review

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

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