GPX8 deficiency–induced oxidative stress reprogrammed m6A epitranscriptome of oral cancer cells

Chen, Xun; Yuan, Linlin; Zhang, Lejia; Chen, Liutao; He, Yi; Wang, Chao; Cheng, Cheng; Chen, Shangwu; Zhao, Wei; Yu, Dongsheng

doi:10.1080/15592294.2023.2208707

Cited by 3 publications

(2 citation statements)

References 59 publications

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“…GPX8, also known as glutathione peroxidase 8, is an enzyme that plays a role in protecting cells from oxidative stress. Oral cancer cells’ m6A epitranscriptome was altered by oxidative stress brought on by GPX8 deficiency( 38 ). By stimulating the Wnt signaling pathway, GPX8 is transcriptionally controlled by FOXC1 and aids in the proliferation of gastric cancer cells( 39 ).…”

Section: Discussionmentioning

confidence: 99%

GPX8 regulates pan-apoptosis in gliomas to promote microglial migration and mediate immunotherapy responses

Chen,

Zheng,

Lin

et al. 2023

Front. Immunol.

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IntroductionGliomas have emerged as the predominant brain tumor type in recent decades, yet the exploration of non-apoptotic cell death regulated by the pan-optosome complex, known as pan-apoptosis, remains largely unexplored in this context. This study aims to illuminate the molecular properties of pan-apoptosis-related genes in glioma patients, classifying them and developing a signature using machine learning techniques.MethodsThe prognostic significance, mutation features, immunological characteristics, and pharmaceutical prediction performance of this signature were comprehensively investigated. Furthermore, GPX8, a gene of interest, was extensively examined for its prognostic value, immunological characteristics, medication prediction performance, and immunotherapy prediction potential. ResultsExperimental techniques such as CCK-8, Transwell, and EdU investigations revealed that GPX8 acts as a tumor accelerator in gliomas. At the single-cell RNA sequencing level, GPX8 appeared to facilitate cell contact between tumor cells and macrophages, potentially enhancing microglial migration. ConclusionsThe incorporation of pan-apoptosis-related features shows promising potential for clinical applications in predicting tumor progression and advancing immunotherapeutic strategies. However, further in vitro and in vivo investigations are necessary to validate the tumorigenic and immunogenic processes associated with GPX8 in gliomas.

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Section: Discussionmentioning

confidence: 99%

GPX8 regulates pan-apoptosis in gliomas to promote microglial migration and mediate immunotherapy responses

Chen,

Zheng,

Lin

et al. 2023

Front. Immunol.

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“…On the contrary, the induction of ferroptosis will lead to changes in m 6 A modification level and m 6 A regulator activity. Our recent research has found that oxidative stress induced by the lack of an important antioxidant gene GPX8 causes reprogramming of the m 6 A epitranscriptome in oral cancer cells [ 104 ]. The m 6 A level of HSCs treated with ferroptosis inducers is enhanced by up-regulating the methyltransferase METTL4 and down-regulating the demethylase FTO [ 100 ].…”

Section: The Regulation Of M 6 a Modification On F...mentioning

confidence: 99%

Regulation of m6A modification on ferroptosis and its potential significance in radiosensitization

Chen,

Zhang,

et al. 2023

Cell Death Discov.

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Radiotherapy is often used to treat various types of cancers, but radioresistance greatly limits the clinical efficiency. Recent studies have shown that radiotherapy can lead to ferroptotic cancer cell deaths. Ferroptosis is a new type of programmed cell death caused by excessive lipid peroxidation. The induction of ferroptosis provides a potential therapeutic strategy for radioresistance. As the most common post-transcriptional modification of mRNA, m6A methylation is widely involved in the regulation of various physiopathological processes by regulating RNA function. Dynamic m6A modification controlled by m6A regulatory factors also affects the susceptibility of cells to ferroptosis, thereby determining the radiosensitivity of tumor cells to radiotherapy. In this review, we summarize the mechanism and significance of radiotherapy induced ferroptosis, analyze the regulatory characteristics of m6A modification on ferroptosis, and discuss the possibility of radiosensitization by enhancing m6A-mediated ferroptosis. Clarifying the regulation of m6A modification on ferroptosis and its significance in the response of tumor cells to radiotherapy will help us identify novel targets to improve the efficacy of radiotherapy and reduce or overcome radioresistance.

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Non-esterified fatty acid palmitate facilitates oxidative endoplasmic reticulum stress and apoptosis of β-cells by upregulating ERO-1α expression

Sharifi,

Yamamoto,

Zeug

et al. 2024

Redox Biology

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GPX8 deficiency–induced oxidative stress reprogrammed m6A epitranscriptome of oral cancer cells

Cited by 3 publications

References 59 publications

GPX8 regulates pan-apoptosis in gliomas to promote microglial migration and mediate immunotherapy responses

GPX8 regulates pan-apoptosis in gliomas to promote microglial migration and mediate immunotherapy responses

Regulation of m6A modification on ferroptosis and its potential significance in radiosensitization

Non-esterified fatty acid palmitate facilitates oxidative endoplasmic reticulum stress and apoptosis of β-cells by upregulating ERO-1α expression

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