GEO series

The m6A methyltransferase METTL14 promotes oncogenic Kras induced juvenile myelomonocytic leukemia through dysregulating autophagy [RNA-seq]

GSE298142 Mus musculus (mouse) RNA-seq (gene expression) 3 samples Submitted 2026/01/21 Platform GPL17021

At a glance

RNA-seq (gene expression) · mouse · 3 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 3 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: The m6A methyltransferase METTL14 promotes oncogenic Kras induced juvenile myelomonocytic leukemia through dysregulating autophagyCell death and differentiation · 2026

Summary (written by the submitters)

The M6A modification plays an important role in the pathogenesis of various myeloid malignancies. However, its specific role in RAS mutant-induced myeloid malignancy is incompletely understood. In this study, we found that m6A methyltransferase METTL14 was highly expressed and associated with a shorter survival in a RAS-mutant myeloid malignancy, juvenile myelomonocytic leukemia (JMML).

Read the full summary ↓

The knockout of METTL14 was revealed to significantly promote hematopoietic stem/progenitor cells (HSPCs) expansion and suppresses disease progression in a KrasG12D/+ mutant-induced mouse model of JMML. Moreover, knockout of METTL14 reduces hyperproliferation of KrasG12D/+ HSPCs and suppresses oncogenic KrasG12D/+-induced myeloid disease in a cell-autonomous manner. Mechanistically, we revealed that the knockout of METTL14 reduced the autophagy levels of HSPCs by suppressing the transcription and translation of autophagy-related genes, such as Atg5 and Atg9a, through m6A modification. Furthermore, we found that the autophagy inhibition through knockout of ATG5 in Kras mutant mice promoted the expansion of HSPCs and inhibited the progression of leukemia disease, consistent with the phenotypes of knockout of METTL14. Finally, we observed that combined treatment with an m6A inhibitor and a MEK inhibitor synergistically suppressed JMML growth. Collectively, these findings highlight the critical role of METTL14 in JMML tumorigenesis and suggest that m6A RNA modification represents a promising therapeutic target for this disease.

Published in

The m6A methyltransferase METTL14 promotes oncogenic Kras induced juvenile myelomonocytic leukemia through dysregulating autophagy

Zhang P, Feng K, Yu X et al. · Cell death and differentiation 2026 · PMID 40819104 · doi:10.1038/s41418-025-01561-0

This dataset

Open GSE298142 in finder → Find more mouse RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE298142_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1268419 and SRA study SRP588110. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40819104) ↗

Samples in this study

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+ 3 more — browse all 3 samples with per-sample file links →

Datasets on a similar topic

GSE298134 The m6A methyltransferase METTL14 promotes oncogenic Kras induced juvenile myelomonocytic leukemia through dysregulating autophagy 12 samples shares mettl14, methyltransferase, myelomonocytic, dysregulating, oncogenic, autophagy, promotes, juvenile
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GSE183403 METTL14 is a chromatin regulator independent of its RNA N6-methyladenosine methyltransferase activity 98 samples shares mettl14, methyltransferase
GSE277667 Cell type-specific apoptosis resistance in juvenile myelomonocytic leukemia 21 samples shares myelomonocytic, juvenile
GSE200103 CK2 phosphorylation of cap methyltransferase CMTR1 promotes RNAPII interaction 12 samples shares methyltransferase, promotes
GSE313425 Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcription [1] 8 samples shares methyltransferase, promotes
GSE313198 Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcription [2] 8 samples shares methyltransferase, promotes
GSE277545 The methyltransferase MLL4 promotes non-alcoholic steatohepatitis by enhancing NF-κB signaling 7 samples shares methyltransferase, promotes

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.