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Histone lactylation drives oncogenesis by facilitating m6A reader protein YTHDF2 expression in ocular melanoma - PubMed
Source: pubmed.ncbi.nlm.nih.gov
Article summary:
1. Histone lactylation is elevated in tumors and is associated with poor prognosis of ocular melanoma.
2. Histone lactylation contributes to tumorigenesis by facilitating YTHDF2 expression, which recognizes the m6A modified PER1 and TP53 mRNAs and promotes their degradation.
3. Target correction of aberrant histone lactylation triggers therapeutic efficacy both in vitro and in vivo, providing novel therapeutic targets for ocular melanoma therapy.
Article analysis:
The article is generally reliable and trustworthy as it provides evidence for its claims through experiments such as immunofluorescence staining, Western blotting, silver staining-mass spectrometry (MS), Kaplan-Meier curves, etc., which are all valid methods to support the findings presented in the article. The authors also provide a conflict of interest statement at the end of the article, indicating that they have no competing interests.
However, there are some potential biases that should be noted when reading this article. Firstly, the authors do not explore any counterarguments or alternative explanations for their findings; instead they focus solely on supporting their own hypothesis without considering other possibilities. Secondly, there is a lack of discussion about possible risks associated with targeting aberrant histone lactylation for ocular melanoma therapy; while this may be due to space constraints in the article, it would be beneficial to include a section discussing potential risks associated with this approach. Finally, while the authors provide evidence for their claims throughout the article, some of these claims could benefit from further exploration or more detailed explanation; for example, more information could be provided about how YTHDF2 recognizes m6A modified PER1 and TP53 mRNAs and promotes their degradation.