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DCBLD2 promotes perivascular anti-tumor immune deprivation by educating SPP1+ pro-angiogenic macrophages

GSE271377 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/07/01 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 × C vs 3 × OE vs 3 × TAM-C vs 3 × TAM-OEGroups 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)
The crosstalk between tumor vasculature and immune microenvironment underpins the anti-tumor effect of anti-angiogenic therapy (AAT) combined with immunotherapy. However, the efficacy improved by AAT in the above combination therapy is limited and its adverse effects are concerning. Integrated transcriptome and surfaceome data identified DCBLD2 as a bipotent molecule on tumor cells as a trigger for abnormal tumor vascular-immune interactions.
Read the full summary ↓
Dcbld2 overexpression accelerated tumor growth through tumor-associated macrophages (TAMs) in preclinical mouse models. Mechanically, DCBLD2 domesticates SPP1+ pro-angiogenic TAMs through ALDH1A3-RXRG-PLK1 axis, constructing TAMs-coated vascular niches that sequester CD8+ T cell infiltration. DCBLD2 expression levels predicted the efficacy of traditional AAT in our lung cancer patient cohorts. Targeting DCBLD2 or ALDH1A3 combined with PD-1 antibody outperformed traditional AAT and immunotherapy combination. Our study identifies DCBLD2 on tumor cells as a checkpoint in abnormal vascular-immune crosstalk, offering a promising target to amplify the potency of vascular normalization and immune activation.
This dataset
Open GSE271377 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 GSE271377_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 PRJNA1131102 and SRA study SRP517658. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
3 × C vs 3 × OE vs 3 × TAM-C vs 3 × TAM-OE

Supports a between-group comparison across 12 samples.

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
Datasets on a similar topic

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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.