METTL3 facilitates immunosurveillance by inhibiting YTHDF2-mediated NLRC5 mRNA degradation in endometrial cancer Article Swipe
Lei Zhan
,
Jing Zhang
,
Junhui Zhang
,
Xiaojing Liu
,
Bao Guo
,
Jiahua Chen
,
Zhenhai Tang
,
Wenyan Wang
,
Qingyuan Wang
,
Bing Wei
,
Yunxia Cao
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1186/s40364-023-00479-4
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1186/s40364-023-00479-4
Background N6-methyladenosine (m6A) methylation is the most abundant chemical posttranscriptional modification of mRNA, and it is associated with the regulation of the immune response to tumors. However, the function of m6A modification in the immune response to endometrial cancer (EC) remains unknown. Our study investigated the immunological role of methyltransferase-like 3 (METTL3) in EC and the underlying molecular mechanism. Methods We investigated the correlation between the expression of METTL3 and CD8 by using an endometrial tissue microarray cohort. Next, we investigated the role and mechanism of METTL3 in the immune response to EC using a mouse tumor model and a CD8 + T cell-EC cell coculture system after METTL3 overexpression or depletion. Additionally, RNA immunoprecipitation (RIP), methylated RIP, and RNA stability experiments were used to investigate the mechanism underlying the function of METTL3 in immunosurveillance of EC. Results METTL3 levels were downregulated in EC patients, low levels of METTL3 were correlated with poor prognosis in EC patients. There was a positive correlation between METTL3 expression and CD8 expression. Overexpression of METTL3 in the EC cell and CD8 + T cell coculture system inhibited EC cell proliferation, migration, and promoted CD8 + T-cell proliferation, and in vivo, METTL3 overexpression increased CD8 + T cell proportions and inhibited EC progression; however, genetic depletion of METTL3 exerted the opposite effects. NLR family CARD domain-containing 5 (NLRC5) was identified as a target of METTL3-mediated m6A modification. The degradation of NLRC5 was increased by YTH domain-containing family 2 (YTHDF2). Conclusions Overall, METTL3, YTHDF2, and NLRC5 have potential to be the diagnostic and prognostic biomarkers for EC. METTL3 facilitated the m6A modifications of NLRC5 and inhibited its degradation through a YTHDF2-dependent mechanism in EC. Genetic overexpression of METTL3 attenuated the immune evasion of EC by promoting NLRC5-mediated immunosurveillance, suggesting that the METTL3/YTHDF2/NLRC5 axis is a promising target of immunotherapy in EC.
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- Type
- letter
- Language
- en
- Landing Page
- https://doi.org/10.1186/s40364-023-00479-4
- https://biomarkerres.biomedcentral.com/counter/pdf/10.1186/s40364-023-00479-4
- OA Status
- gold
- Cited By
- 25
- References
- 11
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4366681336
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Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4366681336Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1186/s40364-023-00479-4Digital Object Identifier
- Title
-
METTL3 facilitates immunosurveillance by inhibiting YTHDF2-mediated NLRC5 mRNA degradation in endometrial cancerWork title
- Type
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letterOpenAlex work type
- Language
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enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-04-21Full publication date if available
- Authors
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Lei Zhan, Jing Zhang, Junhui Zhang, Xiaojing Liu, Bao Guo, Jiahua Chen, Zhenhai Tang, Wenyan Wang, Qingyuan Wang, Bing Wei, Yunxia CaoList of authors in order
- Landing page
-
https://doi.org/10.1186/s40364-023-00479-4Publisher landing page
- PDF URL
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https://biomarkerres.biomedcentral.com/counter/pdf/10.1186/s40364-023-00479-4Direct link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
- OA URL
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https://biomarkerres.biomedcentral.com/counter/pdf/10.1186/s40364-023-00479-4Direct OA link when available
- Concepts
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CD8, Immune system, Cancer research, Immunosurveillance, Cell biology, Cell, Cell growth, Biology, Chemistry, Immunology, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
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25Total citation count in OpenAlex
- Citations by year (recent)
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2025: 10, 2024: 13, 2023: 2Per-year citation counts (last 5 years)
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11Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.promoting | 290 |
| abstract_inverted_index.stability | 121 |
| abstract_inverted_index.Background | 1 |
| abstract_inverted_index.associated | 17 |
| abstract_inverted_index.attenuated | 283 |
| abstract_inverted_index.biomarkers | 259 |
| abstract_inverted_index.correlated | 151 |
| abstract_inverted_index.depletion. | 112 |
| abstract_inverted_index.diagnostic | 256 |
| abstract_inverted_index.expression | 67, 165 |
| abstract_inverted_index.identified | 225 |
| abstract_inverted_index.mechanism. | 59 |
| abstract_inverted_index.methylated | 117 |
| abstract_inverted_index.microarray | 77 |
| abstract_inverted_index.migration, | 187 |
| abstract_inverted_index.prognostic | 258 |
| abstract_inverted_index.regulation | 20 |
| abstract_inverted_index.suggesting | 293 |
| abstract_inverted_index.underlying | 57, 129 |
| abstract_inverted_index.Conclusions | 245 |
| abstract_inverted_index.correlation | 64, 162 |
| abstract_inverted_index.degradation | 234, 272 |
| abstract_inverted_index.endometrial | 38, 75 |
| abstract_inverted_index.experiments | 122 |
| abstract_inverted_index.expression. | 168 |
| abstract_inverted_index.facilitated | 263 |
| abstract_inverted_index.investigate | 126 |
| abstract_inverted_index.methylation | 4 |
| abstract_inverted_index.proportions | 204 |
| abstract_inverted_index.investigated | 45, 62, 81 |
| abstract_inverted_index.modification | 11, 32 |
| abstract_inverted_index.progression; | 208 |
| abstract_inverted_index.Additionally, | 113 |
| abstract_inverted_index.downregulated | 142 |
| abstract_inverted_index.immunological | 47 |
| abstract_inverted_index.immunotherapy | 303 |
| abstract_inverted_index.modification. | 232 |
| abstract_inverted_index.modifications | 266 |
| abstract_inverted_index.NLRC5-mediated | 291 |
| abstract_inverted_index.Overexpression | 169 |
| abstract_inverted_index.overexpression | 110, 198, 280 |
| abstract_inverted_index.proliferation, | 186, 193 |
| abstract_inverted_index.METTL3-mediated | 230 |
| abstract_inverted_index.YTHDF2-dependent | 275 |
| abstract_inverted_index.domain-containing | 221, 241 |
| abstract_inverted_index.N6-methyladenosine | 2 |
| abstract_inverted_index.immunosurveillance | 135 |
| abstract_inverted_index.METTL3/YTHDF2/NLRC5 | 296 |
| abstract_inverted_index.immunoprecipitation | 115 |
| abstract_inverted_index.immunosurveillance, | 292 |
| abstract_inverted_index.posttranscriptional | 10 |
| abstract_inverted_index.methyltransferase-like | 50 |
| cited_by_percentile_year.max | 99 |
| cited_by_percentile_year.min | 94 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 11 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/1 |
| sustainable_development_goals[0].score | 0.41999998688697815 |
| sustainable_development_goals[0].display_name | No poverty |
| citation_normalized_percentile.value | 0.95190319 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |