The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming
Open accessAbstract
N6-methyladenosine (m6A) is a reversible mRNA modification that has been shown to play important roles in various biological processes. However, the roles of m6A modification in macrophages are still unknown. Here, we discover that ablation of Mettl3 in myeloid cells promotes tumour growth and metastasis in vivo. In contrast to wild-type mice, Mettl3-deficient mice show increased M1/M2-like tumour-associated macrophage and regulatory T cell infiltration into tumours. m6A sequencing reveals that loss of METTL3 impairs the YTHDF1-mediated translation of SPRED2, which enhances the activation of NF-kB and STAT3 through the ERK pathway, leading to increased tumour growth and metastasis. Furthermore, the therapeutic efficacy of PD-1 checkpoint blockade is attenuated in Mettl3-deficient mice, identifying METTL3 as a potential therapeutic target for tumour immunotherapy.
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Self-citationFunctional Polarization of Tumour-Associated Macrophages by Tumour-Derived Lactic Acid
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Cited by
Xiong, J., He, J., Zhu, J., Pan, J., Liao, W., Ye, H., Wang, H., Song, Y., Du, Y., Cui, B., et al. (2022) · Molecular Cell · doi:10.1016/j.molcel.2022.02.033 · Cited by 804
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Metadata
- Authors
- Yin, H., Zhang, X., Yang, P., Zhang, X., Peng, Y., Li, D., Yu, Y., Wu, Y., Wang, Y., Zhang, J., Ding, X., Wang, X., Yang, A., & Zhang, R.
- Venue
- Nature Communications
- Published
- 2021-03-02
- Volume
- 12
- Issue
- 1
- Pages
- 1394-1394
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W3134252533
- Cited by
- 404
- References
- 57
- FWCI
- 19.46
- Type
- journal article
- Language
- en
- Open access
- gold
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- Yin, H., Zhang, X., Yang, P., Zhang, X., Peng, Y., Li, D., Yu, Y., Wu, Y., Wang, Y., Zhang, J., Ding, X., Wang, X., Yang, A., & Zhang, R. (2021). RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming. Nature Communications. https://doi.org/10.1038/s41467-021-21514-8
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