m6A Regulatory Gene-Mediated Methylation Modification in Glioma Survival Prediction

Zhang, Guiyun; Zheng, Ping; Lv, Yisong; Shi, Zhijun; Shi, Fei

doi:10.3389/fgene.2022.873764

Cited by 5 publications

(5 citation statements)

References 40 publications

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“…Functional studies have shown that m6A regulator-mediated m6A modification serves a major role in glioma progression (28).…”

Section: Discussionmentioning

confidence: 99%

YTHDF1 promotes the viability and self‑renewal of glioma stem cells by enhancing LINC00900 stability

Zhang,

Zhu,

Zhang

et al. 2024

Int J Oncol

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YTHDF1, an N6-methyladenosine (m6A)-binding protein, is significantly upregulated in glioma tissues. The present study investigated the molecular mechanism underlying the regulatory effects of YTHDF1 on the viability, invasion and self-renewal of glioma stem cells (GSCs). Glioma and normal brain tissues were collected, and reverse transcription-quantitative PCR and western blotting were used to measure the gene and protein expression levels, respectively. Methylated RNA immunoprecipitation-PCR was used to assess the m6A modification level of the target gene. Subsequently GSCs were induced, and YTHDF1 and LINC00900 gene regulation was carried out using lentiviral infection. The viability, invasion and self-renewal of GSCs were assessed by Cell Counting Kit-8, Transwell and sphere formation assays, respectively. Binding between YTHDF1 and LINC00900 was verified by RNA immunoprecipitation and RNA pull-down assays. The targeted binding of microRNA (miR)-1205 to the LINC00900/STAT3 3'-UTR was verified using a luciferase reporter assay. The results revealed that YTHDF1 and LINC00900 expression levels were significantly upregulated in glioma tissues, and a high m6A modification level in LINC00900 transcripts was detected in glioma tissues. Overexpression of YTHDF1 promoted GSC viability, invasion and self-renewal, whereas knockdown of YTHDF1 had the opposite effects. In addition, YTHDF1 maintained the stability of LINC00900 and upregulated its expression through binding to it, thereby promoting GSC viability, invasion and self-renewal. Furthermore, LINC00900 promoted GSC viability, invasion, self-renewal and tumor growth by regulating the miR-1205/STAT3 axis. In conclusion, YTHDF1 promotes GSC viability and self-renewal by regulating the LINC00900/miR-1205/STAT3 axis.

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“…Functional studies have shown that m6A regulator-mediated m6A modification serves a major role in glioma progression (28).…”

Section: Discussionmentioning

confidence: 99%

YTHDF1 promotes the viability and self‑renewal of glioma stem cells by enhancing LINC00900 stability

Zhang,

Zhu,

Zhang

et al. 2024

Int J Oncol

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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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“…More importantly, m6A regulators are abnormally expressed and are extensively involved in the progression of glioma by targeting non-coding RNAs. Moreover, as the most important epigenetic regulators, non-coding RNAs can also affect the function of m6A regulators in glioma [22][23][24]. It has confirmed that m6A can regulate circRNA metabolism, including circRNAs biogenesis, translation, degradation and cellular localization [25].…”

Section: Introductionmentioning

confidence: 87%

Downregulated M6A modification and expression of circRNA_103239 promoted the progression of glioma by regulating the miR-182-5p/MTSS1 signalling pathway

Zhang,

et al. 2023

J. Cancer

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Glioma is a common type of tumor in the central nervous system, and the mortality is high. The prognosis of advanced glioma patients remains poor, and the therapeutic strategies need to be developed. The roles of circRNAs in glioma remain largely unknown. The aim of this study was to explore the functions circRNA_103239 in the biological behaviour changes of glioma cells. The expression of circRNA_103239 in clinical samples and glioma cells were examined using RT-qPCR. The targets of circRNA_103239 were predicted using bioinformatics approach. Gain-and loss-of-function study were carried out. The proliferation of transfected cells were evaluated by CCK-8 assay. Migratory and invasive activities of the cells were examined using wound healing, colony formation and transwell assay. Tumor growth was also evaluated in vivo. The results indicated that the expression of circRNA_103239 was predominantly detected in the cytoplasma of glioma cells. In addition, the expression of circRNA_103239 was down-regulated in glioma, and up-regulated circRNA_103239 inhibited the progression of glioma. Furthermore, miR-182-5p was the novel target of circRNA_103239 in glioma, and MTSS1 was the putative downstream molecule of circRNA_103239/miR-182-5p axis. Additionally, circRNA_103239 suppressed the progression of glioma in a miR-182-5p/MTSS1 dependent manner. Moreover, circRNA_103239 inhibited tumour growth in vivo, and the expression of circRNA_103239 was regulated by METTL14-mediated m6A modification. In summary, in normal cells, METTL14 mediated the m6A modification and expression of circRNA_103239, which sponging miR-182-5p and inducing the expression of MTSS1, subsequently inhibiting the EMT; whereas in glioma cells, downregulated METTL14 induced downregulated m6A modification and expression of circRNA_103239, further resulting in the up-regulation of miR-182-5p and down-regulation of MTSS1, consequently promoting the EMT of glioma cells and triggering the progression of tumor.

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m6A Regulatory Gene-Mediated Methylation Modification in Glioma Survival Prediction

Cited by 5 publications

References 40 publications

YTHDF1 promotes the viability and self‑renewal of glioma stem cells by enhancing LINC00900 stability

YTHDF1 promotes the viability and self‑renewal of glioma stem cells by enhancing LINC00900 stability

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

Downregulated M6A modification and expression of circRNA_103239 promoted the progression of glioma by regulating the miR-182-5p/MTSS1 signalling pathway

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