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TRAIL-induced cytokine production via NFKB2 pathway promotes neutrophil chemotaxis and immune suppression in triple negative breast cancers [MDA-MB-231]

GSE271120 Homo sapiens (human) RNA-seq (gene expression) 17 samples Submitted 2025/05/07 Platform GPL30882
At a glance

RNA-seq (gene expression) · human · 17 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
17 samples: 6 conditions, mostly in triplicateGroups 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.
Paper
TRAIL induces cytokine production via the NFkB2 pathway promoting neutrophil chemotaxis and neutrophil-mediated immune-suppression in triple negative breast cancer cellsCancer letters · 2025
Summary (written by the submitters)
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential cancer therapeutic that selectively induces apoptosis in cancer cells sparing the non-malignant cells. While the effective cytotoxic effect of TRAIL has been demonstrated in vitro, its efficacy in clinical trials has been limited, suggesting a presence of unknown modulatory mechanisms responsible for lack of TRAIL activity in patients.
Read the full summary ↓
We hypothesized that TRAIL treatment elicits transcriptional changes in triple negative breast cancer cells (TNBC) cells that alter the immune milieu. To test this, we performed a RNAseq analysis of MDA-MB-231 cells treated with TRAIL, followed by validation in various TNBC cell lines. We found that TRAIL significantly induces expression of multiple cytokines, such as CXCLs 1, 2, 3, 8,11 and IL-6, which are known to affect neutrophil function. Gene set enrichment analysis (GSEA) indicated a significant enrichment of NFKB pathway. Concordantly, we confirmed that the non-canonical NFKB2 pathway is primarily responsible for induction of these cytokines. We further found that induction of these cytokines was predominantly mediated by death receptor 5 and caspase-8 protein, but not caspase-8 enzymatic activity. CXCLs and IL-6 produced by the TRAIL-treated TNBC cells enhanced chemotaxis of neutrophils isolated from healthy human donors, demonstrating the functional relevance of these cytokines. In vivo, TNBC xenograft tumors grown in mice treated with TRAIL showed an activation of the NFKB2 pathways, elevated production of CXCLs and IL-6, and an increased neutrophil recruitment into the tumors. Moreover, pre-incubation of neutrophils from human donor with supernatants from TRAIL-treated TNBC cells significantly impaired the cytotoxic effect against TNBC cells and showed a reduced respiratory burst. Transcriptomic analysis of neutrophils incubated with either TRAIL alone or supernatant of TRAIL-treated TNBC revealed significant enrichment of expression of inflammatory cytokines, immune modulatory genes, and immune checkpoint genes along with genes having implication on delayed neutrophil apoptosis. Functional studies with these neutrophils confirmed their suppressive effect on T cell proliferation and an increase in Treg suppressive phenotype. Collectively, our study proposes the novel role of TRAIL-induced NFKB2-dependent cytokine production that promotes neutrophil chemotaxis and immune suppression. Our finding suggests that targeting innate immune system may be a promising strategy to improve the efficacy of TRAIL treatment in TNBC.
Published in
TRAIL induces cytokine production via the NFkB2 pathway promoting neutrophil chemotaxis and neutrophil-mediated immune-suppression in triple negative breast cancer cells
Kundu M, Greer YE, Lobanov A et al. · Cancer letters 2025 · PMID 40187604 · doi:10.1016/j.canlet.2025.217692
This dataset
Open GSE271120 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 GSE271120_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 PRJNA1130006 and SRA study SRP517092. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40187604) ↗
Study design
6 conditions, mostly in triplicate
Time pt. 0H, ×3 Time pt.3H, ×3 Time pt.6H, ×3 Time pt.12H, ×3 Time pt.24H, ×3 Time pt.1H, ×2

Supports a between-group comparison across 17 samples.

How we read this: 6 replicated groups read from 17 sample titles; they account for 17 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
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