ArticleOncogene2025
METAP2 inhibits K48-linked ubiquitination of YTHDF2 to promote ovarian cancer progression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Article
- Decoding the crosstalk between ubiquitination and other post-translational modifications in cancer immunity: from mechanisms to clinical prospects.NPJ precision oncology · 2026Review
- Synthesis, characterization, biological evaluation, and molecular modeling of novel nimesulide urea derivatives as potential MetAP2 inhibitors.Scientific reports · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Methionine aminopeptidase 2 (METAP2), one of the two enzymes responsible for removing the N-terminal methionine from nascent proteins, has emerged as a potential drug target for cancer therapy. Yet, its role in ovarian cancer remains largely elusive. Here, we demonstrated that METAP2 is upregulated in ovarian cancer tissues and is associated with poor clinical outcomes. Consistently, METAP2 knockdown significantly suppresses the proliferation and migration of ovarian cancer cells in vivo and in vitro. Mechanistically, co-immunoprecipitation analysis identified YTHDF2 as a key interactor of METAP2. METAP2 interacts with YTHDF2 and attenuates its K48-linked ubiquitination at lysine 245, thereby preventing proteasomal degradation. Importantly, using AlphaFold3 algorithm, we elucidated and then experimentally validated that the Gln342 to Phe361 region of YTHDF2 interacts with the Thr240 to Gly358 region of METAP2. Furthermore, we identified BMF, LXRA, and HIVEP2 as functionally critical downstream targets of the METAP2-YTHDF2 axis, which are essential for ovarian cancer cells proliferation, migration and invasion. Additionally, we validated the therapeutic potential of the METAP2 inhibitor ZGN-1061 in ovarian cancer models. In conclusion, our findings reveal that METAP2 drives ovarian cancer progression by promoting YTHDF2-mediated mRNA decay of BMF/LXRA/HIVEP2, highlighting METAP2 as a potential therapeutic target for ovarian cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.