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Transcriptomic profiling of CRISPR-Cas9 knockout of RAD51D, LIMCH1, and BRD9 in MC38 colorectal cancer cells reveals regulation of PD-L1 expression

GSE324386 Mus musculus (mouse) RNA-seq (gene expression) 29 samples Submitted 2026/03/18 Platform GPL28330
At a glance

RNA-seq (gene expression) · mouse · 29 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
29 samples: 18 × MC38 cells, wildtype, vs 4 × MC38 cells, BRD9 knockout, vs 4 × MC38 cells, LIMCH1 knockout, vs 3 × MC38 cells, RAD51D knockout,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)
Programmed death-ligand 1 (PD-L1) expression in tumor cells plays a critical role in regulating anti-tumor immune responses and determining the efficacy of immune checkpoint blockade therapy. Previous studies have suggested that multiple genes are associated with PD-L1 expression in colorectal cancer, but the underlying regulatory mechanisms remain incompletely understood.
Read the full summary ↓
In this study, we investigated the transcriptional consequences of knocking out three candidate genes, RAD51D, LIMCH1, and BRD9, which were previously identified to be associated with PD-L1 expression in colorectal cancer. Using the murine colorectal cancer cell line MC38, we generated CRISPR-Cas9–mediated knockout cell lines targeting each gene and performed RNA sequencing to characterize the global transcriptomic alterations. Our results revealed that RAD51D deficiency led to activation of the JAK1–STAT1 signaling pathway, accompanied by increased expression of JAK1, STAT1, and IRF1, which are known transcriptional regulators of PD-L1. Consistently, PD-L1 transcription was upregulated following RAD51D knockout. Similar transcriptomic analyses were performed for LIMCH1 and BRD9 knockout cells to explore their potential regulatory roles in PD-L1 expression and tumor immune signaling. This dataset provides a comprehensive transcriptomic resource for understanding how these genes regulate PD-L1 expression and immune-related signaling pathways in colorectal cancer cells, and may facilitate further studies on the molecular mechanisms underlying tumor immune evasion and responses to immune checkpoint blockade.
This dataset
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.

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 GSE324386_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1434532 and SRA study SRP682421. Searching any of these in the dataset finder brings you back here.

Study design
18 × MC38 cells, wildtype, vs 4 × MC38 cells, BRD9 knockout, vs 4 × MC38 cells, LIMCH1 knockout, vs 3 × MC38 cells, RAD51D knockout,

Supports a case/control comparison: 11 samples read as cases, 18 as controls.

How we read this: 4 replicated groups read from 29 sample titles; they account for 29 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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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.