GEO series

N-Myc and STAT Interactor Is A Endometriosis Suppressor Gene

GSE241751 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/08/31 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 12 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: Homo sapiens (human)
Samples: 12 samples: 3 × IHESCs, WT, Vehicle, vs 3 × IHESCs, WT, IFNα treatment, vs 3 × IHESCs, NMI Knockdown, Vehicle , vs 3 × IHESCs, NMI Knockdown, IFNα treatment,Groups are read from the sample names, not from the paper. Check the list below.
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)

Endometriosis is an estrogen-dependent inflammatory disease. A pivotal contributor to endometriosis is the estrogen receptor beta (ERβ), which drives the condition by impeding cell death through interferon (IFN) signaling. One noteworthy component of this cascade is the N-myc and STAT Interactor (NMI), an interferon alpha (IFNα) target gene whose expression is repressed in endometriotic lesions compared to normal endometrium.

Read the full summary ↓

This repression is particularly pronounced in stromal cells, mediated by ERβ. The results of Western blot analyses, comparing IFNα-treated and untreated cells, demonstrate that IFNα treatment triggers cell death signaling, including apoptosis and necroptosis, in endometrial stromal cells. Intriguingly, NMI knockdown (KD) obstructed IFNα-induced cell death signaling in human endometrial stromal cells. Moreover, NMI KD amplified non-canonical IFNα pathways, such as β-Catenin/GSK3β and PI3K/AKT signaling, in endometrial stromal cells following IFNα treatment. RNA sequencing analyses unveiled that NMI KD augmented the expression of genes responsible for cell-cell adhesion and extracellular structural organization in IFNα-independent manners. These findings suggest that NMI KD plays an indispensable role in enhancing the adhesion and invasion of endometriotic cells during endometriosis progression. In summary, NMI functions as an endometriosis suppressor gene in endometriotic stromal cells, curbing the advancement of endometriosis. This intricate interplay of ERβ, IFNα signaling, and NMI offers novel insights into the mechanisms governing endometriosis development.

This dataset

Open GSE241751 in finder → Find more human 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 GSE241751_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 PRJNA1009801 and SRA study SRP457103. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

3 × IHESCs, WT, Vehicle, vs 3 × IHESCs, WT, IFNα treatment, vs 3 × IHESCs, NMI Knockdown, Vehicle , vs 3 × IHESCs, NMI Knockdown, IFNα treatment,

Supports a case/control comparison: 3 samples read as cases, 6 as controls.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM7734753 IHESCs, WT, Vehicle, Replicate 1 IHESCs, WT, Vehicle,
GSM7734754 IHESCs, WT, Vehicle, Replicate 2 IHESCs, WT, Vehicle,
GSM7734755 IHESCs, WT, Vehicle, Replicate 3 IHESCs, WT, Vehicle,
GSM7734756 IHESCs, WT, IFNα treatment, Replicate 1 IHESCs, WT, IFNα treatm…
GSM7734757 IHESCs, WT, IFNα treatment, Replicate 2 IHESCs, WT, IFNα treatm…
GSM7734758 IHESCs, WT, IFNα treatment, Replicate 3 IHESCs, WT, IFNα treatm…
GSM7734759 IHESCs, NMI Knockdown, Vehicle , Replicate 1 IHESCs, NMI Knockdown, …
GSM7734760 IHESCs, NMI Knockdown, Vehicle , Replicate 2 IHESCs, NMI Knockdown, …
GSM7734761 IHESCs, NMI Knockdown, Vehicle , Replicate 3 IHESCs, NMI Knockdown, …
GSM7734762 IHESCs, NMI Knockdown, IFNα treatment, Replicate 1 IHESCs, NMI Knockdown, …
GSM7734763 IHESCs, NMI Knockdown, IFNα treatment, Replicate 2 IHESCs, NMI Knockdown, …
GSM7734764 IHESCs, NMI Knockdown, IFNα treatment, Replicate 3 IHESCs, NMI Knockdown, …

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