Overexpression of CD2/CD27 could inhibit the activation of nitrogen metabolism pathways and suppress M2 polarization of macrophages, thereby preventing brain metastasis of breast cancer

Huang, Guanyou; Wu, Yujuan; Gan, Hongchuan; Chu, Liangzhao

doi:10.1016/j.tranon.2023.101768

Translational Oncology

2023

DOI: 10.1016/j.tranon.2023.101768

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Overexpression of CD2/CD27 could inhibit the activation of nitrogen metabolism pathways and suppress M2 polarization of macrophages, thereby preventing brain metastasis of breast cancer

Guanyou Huang,

Yujuan Wu,

Hongchuan Gan

et al.

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2024

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Cited by 2 publications

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Characterization of the tumor microenvironment in breast cancer brain metastasis

Li,

Lin,

Zhang

et al. 2024

Heliyon

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Characterization of the tumor microenvironment in breast cancer brain metastasis

Li,

Lin,

Zhang

et al. 2024

Heliyon

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Multifaceted bioinformatic analysis of m6A‐related ferroptosis and its link with gene signatures and tumour‐infiltrating immune cells in gliomas

Yang,

Hao,

Guiyang

et al. 2024

J Cellular Molecular Medi

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Whether N6‐Methyladenosine (m6A)‐ and ferroptosis‐related genes act on immune responses to regulate glioma progression remains unanswered. Data of glioma and corresponding normal brain tissues were fetched from the TCGA database and GTEx. Differentially expressed genes (DEGs) were identified for GO and KEGG enrichment analyses. The FerrDb database was based to yield ferroptosis‐related DEGs. Hub genes were then screened out using the cytoHubba database and validated in clinical samples. Immune cells infiltrating into the glioma tissues were analysed using the CIBERSORT R script. The association of gene signature underlying the m6A‐related ferroptosis with tumour‐infiltrating immune cells and immune checkpoints in low‐grade gliomas was analysed. Of 6298 DEGs enriched in mRNA modifications, 144 were ferroptosis‐related; NFE2L2 and METTL16 showed the strongest positive correlation. METTL16 knockdown inhibited the migrative and invasive abilities of glioma cells and induced ferroptosis in vitro. NFE2L2 was enriched in the anti‐m6A antibody. Moreover, METTL16 knockdown reduced the mRNA stability and level of NFE2L2 (both p < 0.05). Proportions of CD8+ T lymphocytes, activated mast cells and M2 macrophages differed between low‐grade gliomas and normal tissues. METTL16 expression was negatively correlated with CD8+ T lymphocytes, while that of NFE2L2 was positively correlated with M2 macrophages and immune checkpoints in low‐grade gliomas. Gene signatures involved in the m6A‐related ferroptosis in gliomas were identified via bioinformatic analyses. NFE2L2 interacted with METTL16 to regulate the immune response in low‐grade gliomas, and both molecules may be novel therapeutic targets for gliomas.

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Overexpression of CD2/CD27 could inhibit the activation of nitrogen metabolism pathways and suppress M2 polarization of macrophages, thereby preventing brain metastasis of breast cancer

Cited by 2 publications

References 61 publications

Characterization of the tumor microenvironment in breast cancer brain metastasis

Characterization of the tumor microenvironment in breast cancer brain metastasis

Multifaceted bioinformatic analysis of m6A‐related ferroptosis and its link with gene signatures and tumour‐infiltrating immune cells in gliomas

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