RETRACTED ARTICLE: N(6)-adenosine-methyltransferase-14 promotes glioma tumorigenesis by repressing argininosuccinate synthase 1 expression in an m6A-dependent manner

Miao, Youqing; Chen, Wei; Zhou, Jianfeng; Shen, Qiyang; Sun, Ying; Li, Tao; Wang, Sheng-Chan

doi:10.1080/21655979.2021.2018386

Cited by 17 publications

(13 citation statements)

References 50 publications

(45 reference statements)

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“…An increasing number of studies have focused on the role of RNA m 6 A methylation in the development of various neurological diseases, such as Parkinson’s disease [ 23 ], Alzheimer’s disease [ 24 , 25 ], multiple sclerosis [ 26 ], tumours [ 27 , 28 , 29 ], epilepsy [ 30 ], and neuropsychiatric disorders [ 31 ]. However, to date, there is limited research focusing on the role of RNA m 6 A methylation in TBI and BGA.…”

Section: Discussionmentioning

confidence: 99%

YTHDF1 Attenuates TBI-Induced Brain-Gut Axis Dysfunction in Mice

Huang

Liu

Zhang

et al. 2023

IJMS

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The brain-gut axis (BGA) is a significant bidirectional communication pathway between the brain and gut. Traumatic brain injury (TBI) induced neurotoxicity and neuroinflammation can affect gut functions through BGA. N6-methyladenosine (m6A), as the most popular posttranscriptional modification of eukaryotic mRNA, has recently been identified as playing important roles in both the brain and gut. However, whether m6A RNA methylation modification is involved in TBI-induced BGA dysfunction is not clear. Here, we showed that YTHDF1 knockout reduced histopathological lesions and decreased the levels of apoptosis, inflammation, and oedema proteins in brain and gut tissues in mice after TBI. We also found that YTHDF1 knockout improved fungal mycobiome abundance and probiotic (particularly Akkermansia) colonization in mice at 3 days post-CCI. Then, we identified the differentially expressed genes (DEGs) in the cortex between YTHDF1-knockout and WT mice. These genes were primarily enriched in the regulation of neurotransmitter-related neuronal signalling pathways, inflammatory signalling pathways, and apoptotic signalling pathways. This study reveals that the ITGA6-mediated cell adhesion molecule signalling pathway may be the key feature of m6A regulation in TBI-induced BGA dysfunction. Our results suggest that YTHDF1 knockout could attenuate TBI-induced BGA dysfunction.

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Section: Discussionmentioning

confidence: 99%

YTHDF1 Attenuates TBI-Induced Brain-Gut Axis Dysfunction in Mice

Huang

Liu

Zhang

et al. 2023

IJMS

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“…Accumulating evidence has revealed the unique role of m6A RNA methylation in the genesis and development of cancer including glioma. A series of studies using the knockdown model of METTL3 and METTL14 observed a reduction of m6A extent accompanied by upregulation of oncogenes and downregulation of tumor suppressors [20,21] . On the contrary, overexpression of METTL3 leads to decreased proliferation and migration of glioma cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of N6-Methyladenosine-Related Gene Based Prognostic Signature to Predict Survival and Potential Therapeutic Drugs in Glioma

Dong

Zhang

Fang

et al. 2022

Preprint

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N6-methyladenosine (m6A) modification is one of the most abundant RNA modification methods in the eukaryote. It was reported that abnormal expression of m6A-related genes is closely associated with the tumorigenesis and progression of glioma. However, the role of m6A RNA methylation in the development of glioma is still unclear. In the current study, we defined m6A-related clusters in glioma cohorts from The Cancer Genome Atlas (TCGA) database which exhibited distinct outcomes in OS. From differentially expressed genes between these clusters, m6A-associated prognostic genes were further narrowed down. Eventually, FRA10AC1, GPR85, MARCHF5, and NUAK2 were selected to form the m6Amethylation-based prognostic signature (MMS) of glioma by Cox and LASSO regression analysis. Subsequently, the efficacy and effectiveness of MMS were examined in the training, testing, and whole groups. Kaplan-Meier survival curve indicated high- and low-risk subgroups divided by MMS showed significantly different OS, and the AUCs of MMS reached 0.75 in all groups. In combined analysis with other clinical-pathological factors, MMS was proved as an independent predictive standard of glioma prognosis. In addition, gene enrichment revealed changes in signaling pathways, biological processes and hallmark gene sets between high- and low-risk subgroups. Last but not least, potential therapeutic molecules for the high-risk patient with MMS were subsequently explored. In general, our study provided MMS, a novel molecular panel closely associated with m6A methylation that holds high efficacy in predicting the prognosis of glioma.

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“…Methyltransferase 14 (METTL14), a RNA N6-adenosine methyltransferase, participates in tumor development via modulating RNA function (Chen et al, 2020). ASS1 is a target of METTL14mediated N6-methyladenosine modification (Miao et al, 2022). Specifically, METTL14 upregulation increases mRNA m6A modification of ASS1 and suppresses ASS1 transcriptional expression.…”

Section: Ass1 Regulation and Signaling Networkmentioning

confidence: 99%

Argininosuccinate synthase 1, arginine deprivation therapy and cancer management

Sun

Zhao

2022

Front. Pharmacol.

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Metabolic reprogramming is an emerging hallmark of tumor cells. In order to survive in the nutrient-deprived environment, tumor cells rewire their metabolic phenotype to provide sufficient energy and build biomass to sustain their transformed state and promote malignant behaviors. Amino acids are the main compositions of protein, which provide key intermediate substrates for the activation of signaling pathways. Considering that cells can synthesize arginine via argininosuccinate synthase 1 (ASS1), arginine is regarded as a non-essential amino acid, making arginine depletion as a promising therapeutic strategy for ASS1-silencing tumors. In this review, we summarize the current knowledge of expression pattern of ASS1 and related signaling pathways in cancer and its potential role as a novel therapeutic target in cancer. Besides, we outline how ASS1 affects metabolic regulation and tumor progression and further discuss the role of ASS1 in arginine deprivation therapy. Finally, we review approaches to target ASS1 for cancer therapies.

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RETRACTED ARTICLE: N(6)-adenosine-methyltransferase-14 promotes glioma tumorigenesis by repressing argininosuccinate synthase 1 expression in an m6A-dependent manner

Cited by 17 publications

References 50 publications

YTHDF1 Attenuates TBI-Induced Brain-Gut Axis Dysfunction in Mice

YTHDF1 Attenuates TBI-Induced Brain-Gut Axis Dysfunction in Mice

Identification of N6-Methyladenosine-Related Gene Based Prognostic Signature to Predict Survival and Potential Therapeutic Drugs in Glioma

Argininosuccinate synthase 1, arginine deprivation therapy and cancer management

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