METTL3 restrains papillary thyroid cancer progression via m6A/c-Rel/IL-8-mediated neutrophil infiltration

He, Jing; Zhou, Mingxia; Yin, Jie; Wan, Junhu; Chu, Jie; Jia, Jinlin; Sheng, Jinxiu; Wang, Chang; Yin, Hang; He, Fucheng

doi:10.1016/j.ymthe.2021.01.019

Cited by 110 publications

(75 citation statements)

References 39 publications

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“…The activation of Wnt/β-catenin signaling has been reported plenty of times in DLBCL. For instance, GPNMB was suggested to be an oncogene in DLBCL, revealed by partly activating the Wnt/β-catenin signaling via YAP1 [ 44 ]. The downregulation of another pair of oncogenes in DLBCL, FBN1, and TIMP1 resulted in the downregulation of Wnt3, GSK3β, β-catenin, c-Myc, and cyclin D1, suggesting the inactivation of Wnt/β-catenin signaling [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Knockdown of zinc finger protein 267 suppresses diffuse large B-cell lymphoma progression, metastasis, and cancer stem cell properties

et al. 2022

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Zinc finger protein 267 (ZNF267) is a member of the Kruppel-like transcription factor family, which regulates various biological processes such as cell proliferation and differentiation. However, the biological significance of ZNF267 and its potential role in diffuse large B-cell lymphoma (DLBCL) remain to be documented. Experiments were herein conducted to study the role of ZNF267 in DLBCL. real-time quantitative reverse transcription PCR and Western blotting assays were conducted to detect the expression of ZNF267 in tissues and cells. Tissue microarray and bioinformatics analyses of public data were also done to detect the expression status and clinical significance of ZNF267. Functional cell experiments including CCK8 assay, colony formation assay, 5-ethynyl-2ʹ-deoxyuridine (EDU) assay, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) assay, transwell assay, and wound healing assay were conducted to study the effects of ZNF267 knockdown and overexpression on cell proliferation and mobility. Xenograft assay was also conducted to confirm the effects of ZNF267 knockdown in vivo . In the present study, we found ZNF267 was significantly upregulated in DLBCL and predicted a poor survival outcome based on the bioinformatics analysis. Functionally, the knockdown of ZNF267 resulted in less cell proliferation and mobility, whereas the overexpression led to enhanced cell proliferation and mobility. Animal experiments also confirmed that ZNF267 silence contributed to less tumor growth and less lung metastasis. Further analysis showed that ZFN267 knockdown resulted in decreased epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties. Our results suggest that ZNF267 is an oncogene in DLBCL and its silence could compromise the aggression of DLBCL, which makes ZNF267 a promising therapeutic target.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Knockdown of zinc finger protein 267 suppresses diffuse large B-cell lymphoma progression, metastasis, and cancer stem cell properties

et al. 2022

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“…In addition, neutrophils and activated memory CD4 T cells were more highly expressed in CD and UC tissues than in normal tissues, but no significant differences in the T cell types or neutrophils exist between the two m 6 A modification patterns, indicating that m 6 A regulators may influence inflammation development primarily by recruiting macrophages. METTL3 deficiency increases the secretion of IL8 and elevates the recruitment of neutrophils (He et al, 2021). In our study, IL8 expression in m 6 Acluster1 was increased, and expression of IL15, IL16, and IL18 was upregulated in m 6 Acluster2, suggesting that m 6 A methylation modification may change mucosal inflammatory factors in IBD.…”

Section: Discussionsupporting

confidence: 53%

m6A Modification Mediates Mucosal Immune Microenvironment and Therapeutic Response in Inflammatory Bowel Disease

Chen

Lei

2021

Front. Cell Dev. Biol.

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Accumulating evidence links m6A modification with immune infiltration. However, the correlation and mechanism by which m6A modification promotes intestinal immune infiltration in inflammatory bowel disease (IBD) is unknown. Here, genomic information from IBD tissues was integrated to evaluate disease-related m6A modification, and the correlation between the m6A modification pattern and the immune microenvironment in the intestinal mucosa was explored. Next, we identified hub genes from the key modules of the m6Acluster and analyzed the correlation among the hub genes, immune infiltration, and therapy. We found that IGF2BP1 and IGF2BP2 expression was decreased in Crohn’s disease (CD) tissues and that IGF2BP2 was decreased in ulcerative colitis (UC) tissues compared with normal tissues (P < 0.05). m6Acluster2, containing higher expressions of IL15, IL16, and IL18, was enriched in M0 macrophage, M1 macrophage, native B cells, memory B cells, and m6Acluster1 with high expression of IL8 and was enriched in resting dendritic and plasma cells (P < 0.05). Furthermore, we reveal that expression of m6A phenotype-related hub genes (i.e., NUP37, SNRPG, H2AFZ) was increased with a high abundance of M1 macrophages, M0 macrophages, and naive B cells in IBD (P < 0.01). Immune checkpoint expression in the genecluster1 with higher expression of hub genes was increased. The anti-TNF therapeutic response of patients in genecluster1 was more significant, and the therapeutic effect of CD was better than that of UC. These findings indicate that m6A modification may affect immune infiltration and therapeutic response in IBD. Assessing the expression of m6A phenotype-related hub genes might guide the choice of IBD drugs and improve the prediction of therapeutic response to anti-TNF therapy.

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“…METTL3 and METTL14 were the hub nodes of the m6A writers, and the hub node of the reader was HNRNPA2B1. Recently, He et al ( He et al, 2021 ) demonstrated that METTL3 regulates tumor growth by cooperating with YTHDF2. This is to some extent a validation of our prediction.…”

Section: Resultsmentioning

confidence: 99%

The Role of m6A Regulator-Mediated Methylation Modification and Tumor Microenvironment Infiltration in Glioblastoma Multiforme

Wang

Cao

Zhong

et al. 2022

Front. Cell Dev. Biol.

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N6-methyladenosine (m6A) RNA methylation is an emerging epigenetic modification in recent years and epigenetic regulation of the immune response has been demonstrated, but the potential role of m6A modification in GBM tumor microenvironment (TME) cell infiltration and stemness remain unknown. The m6A modification patterns of 310 GBM samples were comprehensively evaluated based on 21 m6A regulators, and we systematically correlated these modification patterns with TME cell infiltration characteristics and stemness characteristics. Construction of m6Ascore to quantify the m6A modification patterns of individual GBM samples using a principal component analysis algorithm. We identified two distinct patterns of m6A modification. The infiltration characteristics of TME cells in these two patterns were highly consistent with the immunophenotype of the GBM, including the immune activation differentiation pattern and the immune desert dedifferentiation pattern. We also identified two modes of regulation of immunity and stemness by m6A methylation. Stromal activation and lack of effective immune infiltration were observed in the high m6Ascore subtype. Pan-cancer analysis results illustrate a significant correlation between m6AScore and tumor clinical outcome, immune infiltration, and stemness. Our work reveals that m6A modifications play an important role in the development of TME and stemness diversity and complexity. Patients with a low m6AScore showed significant therapeutic advantages and clinical benefits. Assessing the m6A modification pattern of individual tumors will help enhance our knowledge of TME infiltration and stemness characteristics, contribute to the development of immunotherapeutic strategies.

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METTL3 restrains papillary thyroid cancer progression via m6A/c-Rel/IL-8-mediated neutrophil infiltration

Cited by 110 publications

References 39 publications

RETRACTED ARTICLE: Knockdown of zinc finger protein 267 suppresses diffuse large B-cell lymphoma progression, metastasis, and cancer stem cell properties

RETRACTED ARTICLE: Knockdown of zinc finger protein 267 suppresses diffuse large B-cell lymphoma progression, metastasis, and cancer stem cell properties

m6A Modification Mediates Mucosal Immune Microenvironment and Therapeutic Response in Inflammatory Bowel Disease

The Role of m6A Regulator-Mediated Methylation Modification and Tumor Microenvironment Infiltration in Glioblastoma Multiforme

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