m6A RNA methylation regulators could contribute to the occurrence of chronic obstructive pulmonary disease

Huang, Xinwei; Lv, Dongjin; Yang, Xiao; Li, Min; Zhang, Hong

doi:10.1111/jcmm.15848

Cited by 56 publications

(53 citation statements)

References 49 publications

(128 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Certain studies have reported that METTL3 contributes to transforming growth factor-β-induced epithelial-mesenchymal transition of lung cancer cells (39). An additional study revealed that there is a significant correlation between METTL3 expression and the occurrence of chronic obstructive pulmonary disease (40). However, the role of METTL3-mediated m6A modification in NSCLC initiation and progression is not fully known.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2021

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Subsequently, the connectivity per gene was deduced through calculating connection strengths with other genes. After validating the module structure preservation using the module preservation R function, the gene expression profile of each module was summarized by the module eigengene on whom IPF traits were regressed in the Limma R package ( Huang et al, 2020 ). The IPF-related module was selected with the highest coefficient square (r 2 ) and the p value <0.001.…”

Section: Methodsmentioning

confidence: 99%

Identification of Hub Genes and Pathways Associated With Idiopathic Pulmonary Fibrosis via Bioinformatics Analysis

Wan

Huang

Cong

et al. 2021

Front. Mol. Biosci.

Self Cite

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is a progressive disease whose etiology remains unknown. The purpose of this study was to explore hub genes and pathways related to IPF development and prognosis. Multiple gene expression datasets were downloaded from the Gene Expression Omnibus database. Weighted correlation network analysis (WGCNA) was performed and differentially expressed genes (DEGs) identified to investigate Hub modules and genes correlated with IPF. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and protein-protein interaction (PPI) network analysis were performed on selected key genes. In the PPI network and cytoHubba plugin, 11 hub genes were identified, including ASPN, CDH2, COL1A1, COL1A2, COL3A1, COL14A1, CTSK, MMP1, MMP7, POSTN, and SPP1. Correlation between hub genes was displayed and validated. Expression levels of hub genes were verified using quantitative real-time PCR (qRT-PCR). Dysregulated expression of these genes and their crosstalk might impact the development of IPF through modulating IPF-related biological processes and signaling pathways. Among these genes, expression levels of COL1A1, COL3A1, CTSK, MMP1, MMP7, POSTN, and SPP1 were positively correlated with IPF prognosis. The present study provides further insights into individualized treatment and prognosis for IPF.

show abstract

“…The function of m6A-modified targets is executed by m6A binding proteins (readers) through binding to m6A directly or indirectly, including YTH N6-methyladenosine RNA-binding proteins, YTH domain-containing proteins, IGF2BPs, and HNRNP protein families ( Tong et al, 2018 ). These writers, erasers, and readers, serving as m6A RNA methylation regulators, can influence mRNA of target gene at different levels, including nuclear export, translation, splicing, stability, and decay ( Lan et al, 2019 ; Huang et al, 2020 ; Nombela et al, 2021 ) and have important influences in diverse physiological and pathological processes, such as cell proliferation and differentiation, oncogenic protein expression, and the proliferation, survival, initiation, and progression of tumor cell ( Figure 1A ; Chen et al, 2019 ; Lan et al, 2019 ; Du et al, 2020 ; Huang et al, 2020 ; Nombela et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Identification of the Role and Clinical Prognostic Value of Target Genes of m6A RNA Methylation Regulators in Glioma

Cong

Huang

et al. 2021

Front. Cell Dev. Biol.

Self Cite

View full text Add to dashboard Cite

m6A RNA methylation regulators can regulate the growth, progression, and invasion of glioma cells by regulating their target genes, which provides a reliable support for the m6A regulator–target axes as the novel therapeutic targets and clinical prognostic signature in glioma. This study aimed to explore the role and prognostic value of m6A RNA methylation regulators and their targets. Expression profiles and clinicopathological data were obtained from the Chinese Glioma Genome Atlas (CGGA), The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Clinical Proteome Tumor Analysis Consortium (CPTAC) datasets. Differential expression and correlation analyses were performed between normal and glioma tissues at mRNA and protein levels. Univariate Cox regression, survival, and Lasso Cox regression analyses were conducted to identify and establish the prognostic gene signature. Kaplan–Meier curve, multivariate Cox regression analysis, and ROC were utilized to evaluate the prognostic capacity of the prognostic gene signature. The correlation analysis, systematic bioinformatics analysis, and cell experiment were performed to further understand the potential underlying molecular mechanisms and drug sensitivity. Our results suggested that IGF2BP2, KIAA1429, METTL16, and METTL3, as well as 208 targets are involved in the occurrence of glioma, GBM, and LGG. YTHDF1 and 78 targets involved the occurrence of glioma and GBM, not LGG, among which 181 genes were associated with overall survival. From other findings and our cell experiment results, we demonstrated that METTL3 can activate Notch pathway and facilitate glioma occurrence through regulating its direct targets NOTCH3, DLL3, and HES1, and Notch pathway genes may serve as the potential treatment targets for glioma. Our study established and validated a seven-gene signature comprising METTL3, COL18A1, NASP, PHLPP2, TIMP1, U2AF2, and VEGFA, with a good capability for predicting glioma survival, which may guide therapeutic customization and clinical decision-making. These genes were identified to influence 81 anticancer drug responses, which further contributes to the early phase clinical trials of drug development.

show abstract

m6A RNA methylation regulators could contribute to the occurrence of chronic obstructive pulmonary disease

Cited by 56 publications

References 49 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

Identification of Hub Genes and Pathways Associated With Idiopathic Pulmonary Fibrosis via Bioinformatics Analysis

Identification of the Role and Clinical Prognostic Value of Target Genes of m6A RNA Methylation Regulators in Glioma

Contact Info

Product

Resources

About