ArticleHuman cell2025
METTL14 knockdown augmented the polarization of M2-like macrophages to promote acute myeloid leukemia progression.
Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Within the m6A methyltransferase complex, methyltransferase-like 14 (METTL14) constitutes a pivotal component. This study aims to elucidate the role of METTL14 in macrophage differentiation and its involvement in the progression of acute myeloid leukemia (AML) through the modulation of programmed cell death-ligand 1 (PD-L1) expression in M2-like macrophages. The expression levels of METTL14 in M1-like and M2-like macrophages were quantified using real-time quantitative polymerase chain reaction (QRT-PCR). Macrophage differentiation in THP-1 cells was induced via treatment with phorbol 12-myristate 13-acetate (PMA), followed by lentiviral-mediated overexpression or knockdown of METTL14. Changes in the expression of CD86, iNOS, Arg-1, and CD206 were evaluated. The effects of METTL14 knockdown and overexpression on macrophage differentiation, M2 macrophage proliferation, and apoptosis was assessed. AML cells were co-cultured with M2 macrophages subjected to either METTL14 knockdown or overexpression, and subsequent changes in AML cell proliferation, apoptosis, migration, invasion, and m6A methylation levels were investigated. The expression of METTL14 mRNA was elevated in M1-like macrophages. Knockdown of METTL14 resulted in a significantly reduction in the expression of M1 markers, such as CD86 and iNOS, while concurrently increasing the expression of M2 markers, including Arg-1 and CD206. Additionally, the depletion of METTL14 facilitated the proliferation of M2-like macrophages, inhibited apoptosis, and decreased phagocytic capacity. Conversely, overexpression of METTL14 yielded opposite outcomes. Co-culture experiments demonstrated that M2-like macrophages with METTL14 knockdown significantly promoted the proliferation of AML cell, suppressed apoptosis, and enhanced migration and invasion. Concurrently, cellular m6A levels were elevated. Treatment with anti-PD-L1 partially reversed the effects of METTL14 knockdown. These findings suggest that METTL14 may enhance the proliferation of AML cells while inhibiting apoptosis by influencing macrophage differentiation and modulating macrophage function, with these effects being associated with YTHDF1 and PD-L1.
Indexed as
Identifiers
41026373What OpenQuestion holds
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.