GEO series

STAT1-GCLM axis promotes B-cell expansion in adenoid hypertrophy

GSE329298 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/06/30 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 9 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: 9 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.

Summary (written by the submitters)

Adenoid hypertrophy (AH) is a chronic inflammatory disorder characterized by pathological enlargement of nasopharyngeal lymphoid tissue, yet the mechanisms driving its progression remain unclear. Here, an LPS-induced inflammatory model was established in human immortalized B lymphoblastoid cells (B-LCLs). LPS stimulation increased IL-6 and TNF-α secretion and enhanced Ki67 expression, indicating an activated proliferative phenotype.

Read the full summary ↓

RNA-seq analysis revealed marked transcriptional reprogramming, with significant enrichment of STAT signaling, glutathione metabolism, and ferroptosis-related pathways. Further experiments showed that inflammatory stimulation promoted STAT1 phosphorylation and nuclear translocation, whereas pharmacological inhibition of STAT signaling suppressed B-cell proliferation and partially reversed the inflammatory transcriptional program. Functionally, STAT inhibition partially reduced ATP production but further increased ROS accumulation, suggesting that STAT signaling contributes to both metabolic activation and redox maintenance. Mechanistically, GCLM was identified as a downstream target of STAT1 through differential gene overlap analysis and was validated by qPCR, western blotting, clinical sample analysis, and ChIP-qPCR. GCLM expression was elevated in the inflammatory model and in stage IV AH tissues, while STAT inhibition reduced GSH levels and enhanced ferroptosis-related changes. Consistently, GCLM knockdown decreased GSH content, increased lipid peroxidation, and altered ferroptosis-associated protein expression. Collectively, these findings demonstrate that the STAT1-GCLM axis sustains glutathione-dependent redox homeostasis and suppresses ferroptosis in B cells, thereby promoting AH progression.

This dataset

Open GSE329298 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 GSE329298_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 PRJNA1458585 and SRA study SRP695526. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 9 more — browse all 9 samples with per-sample file links →

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