HBXIP promotes gastric cancer via METTL3-mediated MYC mRNA m6A modification

Yang, Zhi; Jiang, Xiaodi; Liu, Deming; Jiang, Xiaofeng

doi:10.18632/aging.103767

Cited by 51 publications

(48 citation statements)

References 33 publications

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“…Furthermore, METTL3 and Bcl-2 expression levels were positively correlated. Certain studies have revealed that METTL3 overexpression directly mediates m6A methylation and inhibits apoptosis in various types of cancer (42,43). For example, overexpression of Bcl-2 blocks adriamycin-induced apoptosis in bladder cancer cells (44).…”

Section: Discussionmentioning

confidence: 99%

METTL3‑mediated m6A modification of Bcl‑2 mRNA promotes non‑small cell lung cancer progression

et al. 2021

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Methyltransferase-like 3 (METTL3) is an RNA methyltransferase that mediates modification of N6-methyladenosine (m6A), which serves as an oncogene in various types of cancer. The role of m6A modification in the onset and progression of cancer has attracted growing attention. However, the functional and regulatory mechanisms of METTL3 in non-small cell lung cancer (NSCLC) progression are still poorly understood. In the present study, METTL3 expression in NSCLC tissue was analyzed using the Gene Expression Profiling Interactive Analysis database. Western blotting and reverse transcription-quantitative PCR were performed to evaluate the expression of METTL3 in NSCLC tissue and cell lines. Here, knockdown and overexpression of METTL3 notably decreased NSCLC cell viability, apoptosis and migration in vitro and, as well as tumorigenicity in vivo. Expression of METTL3 was upregulated in NSCLC tissue. METTL3 overexpression promoted cell viability and migration in NSCLC, while knockdown of METTL3 yielded the opposite result in vivo and in vitro. METTL3 increased Bcl-2 translation via m6A modification, which increased viability and enhanced migration of NSCLC cells. METTL3 served as an oncogene in NSCLC via METTL3-mediated Bcl-2 mRNA m6A modification, which indicated that targeting METTL3 may be an effective therapeutic strategy for clinical management of NSCLC.

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Section: Discussionmentioning

confidence: 99%

METTL3‑mediated m6A modification of Bcl‑2 mRNA promotes non‑small cell lung cancer progression

et al. 2021

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“…Some lncRNAs were highly expressed in tumor tissues, while others were highly expressed in normal tissues (P < 0.05). It has been reported that HBXIP is upregulated in cancers, which plays a role as a tumor promoter in cancer via driving metabolic reprogramming through METTL3-mediated m6A modification [ 19 ]. Lately, it has been shown that HBXIP might promote the development of gastric cancer, which is m6A-modified [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

N6-Methyladenosine Related Long Non-Coding RNAs and Immune Cell Infiltration in the Tumor Microenvironment of Gastric Cancer

Zhu

2021

Biol Proced Online

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Aim To illustrate the influence of N6-methyladenosine long non-coding RNAs and immune cell infiltration in gastric cancer. Methods We downloaded workflow-type data and clinical data from The Cancer Genome Atlas project. The relationship of lncRNA and m6A was identified. Kyoto Encyclopedia of Genes and Genomes gene expression enrichment analysis was performed. Lasso regression was utilized to construct a prognostic model. Survival analysis to explore the relationship between m6A lncRNA and clinical survival data. Differential analysis of the tumor microenvironment and immune correlation analysis to determine immune cell infiltration levels and their correlation with clinical prognosis. Results Co-expression analysis indicated that lncRNA expression was associated closely with m6A. m6A-lncRNAs were partially highly expressed in tumor tissue and could be used in a prognostic model to predict GC prognosis, independent of other clinical characteristics. “ADIPPOCYTOKINE SIGNALING PATHWAY” was most significantly enriched according to GSEA. ACBD3-AS1 was overexpressed in tumor tissue. Naïve B cell, Plasma cells, resting CD4 memory T cell were highly infiltrated tissues in cluster 2, while Macrophages M2, resting Mast cells, Monocytes, regulates T cells were lowly in cluster 1. All related scores were higher in cluster 2, indicating a lower purity of tumor cells and higher density of immune-related cells in the tumor microenvironment. Conclusion m6A lncRNA is closely related to the occurrence and progression of GC. The corresponding prognostic model can be utilized to evaluate the prognosis of GC. m6A lncRNA and related immune cell infiltration in the tumor microenvironment can provide novel therapeutic targets for further research.

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“…METTL3 is the core of m6A modification, and changes in the levels or methylation function of METTL3 have been found in the progress of many diseases, so METTL3 function and level abnormalities are often important research points. The correlation research of METTL3 in GC is not exceptional, and most results have shown that increased METTL3 levels promote the progression of GC [11,[39][40][41].…”

Section: Discussionmentioning

confidence: 99%

Inhibiting PP2Acα Promotes the Malignant Phenotype of Gastric Cancer Cells through the ATM/METTL3 Axis

Cheng

Gao

Liang

et al. 2021

BioMed Research International

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This article is aimed at exploring the relationship between the phosphatase 2A catalytic subunit Cα (PP2Acα, encoded by PPP2CA) and methyltransferase-like 3 (METTL3) in the malignant progression of gastric cancer (GC). Through analyzing the bioinformatics database and clinical tissue immunohistochemistry results, we found that abnormal PP2Acα and METTL3 levels were closely related to the malignant progression of GC. To explore the internal connection between PP2Acα and METTL3 in the progression of GC, we carried out cellular and molecular experiments and finally proved that PP2Acα inhibition can upregulate METTL3 levels by activating ATM activity, thereby promoting the malignant progression of GC.

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HBXIP promotes gastric cancer via METTL3-mediated MYC mRNA m6A modification

Cited by 51 publications

References 33 publications

METTL3‑mediated m6A modification of Bcl‑2 mRNA promotes non‑small cell lung cancer progression

METTL3‑mediated m6A modification of Bcl‑2 mRNA promotes non‑small cell lung cancer progression

N6-Methyladenosine Related Long Non-Coding RNAs and Immune Cell Infiltration in the Tumor Microenvironment of Gastric Cancer

Inhibiting PP2Acα Promotes the Malignant Phenotype of Gastric Cancer Cells through the ATM/METTL3 Axis

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