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Splicing inhibition hampers pancreatic cancer cell viability by disrupting DNA repair proficiency and mitotic checkpoint integrity

GSE312205 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/07/29 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)
Topic
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
12 samples: 3 × PANC1 PDAC cells treated with DMSO, vs 3 × PANC1 PDAC cells treated for 6 hours with 3.3 nM Pladienolide B, vs 3 × PANC1 PDAC cells treated for 8 hours with 500 nM Thailastatin A, vs 3 × PANC1 PDAC cells treated for 12 hours with 3.3 mM Indisulam,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)
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a remarkably poor prognosis. Splicing dysregulation is emerging as a hallmark of cancer, influencing multiple aspects of tumor development. To evaluate the impact of its dysregulation we employed three splicing-targeting drugs: Pladienolide B (PdB), Thailanstatin A (Th.A) and Indisulam (Ind.), all involved in the recognition of 3’ splice site.
Read the full summary ↓
Transcriptome analyses in PDAC cell lines and PDOs revealed that splicing inhibition negatively affects the DDR pathway (BRCA1, CHEK1, CHEK2) in homologous recombination-proficient (HRP) PDAC models, representing a promising strategy to enhance their sensitivity to PARP inhibitor (Talazoparib) treatment. Moreover, among the genes that are altered by all three drugs, we observe an enrichment of genes involved in the mitotic checkpoint genes (AURKA, AURKB, CDC25B, KIF21, EZH2). Indeed, splicing inhibitors induced severe mitotic defects with a strong enrichment in the G2/M phase of the cycle, leading to the accumulation of condensed chromosomes on monopolar spindles and misaligned chromosomes on bipolar spindles; which lead to the formation of multinucleated cells. The high expression of AURKA, AURKB and CHEK1 were correlated with poor prognosis in PDAC; furthermore, CHEK1 expression was also significantly correlated with AURKA and AURKB. Indeed, combined treatments with CHEK1i (AZD7762) and AURKAi (Alisertib) have an additive effect on both PDAC cell lines and PDOs, suggesting promising new therapeutic strategies that may be used in PDAC patients.
This dataset
Open GSE312205 in finder → Find more human RNA-seq datasets → Pancreatic cancer landscape →
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 GSE312205_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 PRJNA1372665 and SRA study SRP650709. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
3 × PANC1 PDAC cells treated with DMSO, vs 3 × PANC1 PDAC cells treated for 6 hours with 3.3 nM Pladienolide B, vs 3 × PANC1 PDAC cells treated for 8 hours with 500 nM Thailastatin A, vs 3 × PANC1 PDAC cells treated for 12 hours with 3.3 mM Indisulam,

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
More Pancreatic cancer datasets

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