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CDK16 and CDK18 inhibition suppresses nuclear pore-mediated DNA repair and hepatocellular carcinoma [liver tumor]

GSE300751 Mus musculus (mouse) RNA-seq (gene expression) 14 samples Submitted 2026/03/10 Platform GPL34328
At a glance

RNA-seq (gene expression) · mouse · 14 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
14 samples: 5 × HCC, CDK18KO, vs 5 × HCC, WT, vs 4 × HCC, CDK16KO CDK18KO,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)
Inhibition of cyclin-dependent kinases (CDK) 4 and 6 has become part of the current standard-of-care treatment in advanced estrogen receptor-positive breast cancer. However, many tumor types are resistant to current CDK inhibitors and the therapeutic value of other CDK family members remains to be validated. By using gene-editing techniques in human cancer cells and genetically-modified mouse models we report here that MYC and beta-catenin driven hepatocellular carcinoma (HCC) is sensitive to the inactivation of CDK16 and CDK18.
Read the full summary ↓
Whereas individual ablation of CDK14-18 subfamily members displays little effect, concomitant genetic ablation or pharmacological inhibition of CDK16 and CDK18 results in proliferative arrest accompanied by DNA damage and apoptotic cell death. Mechanistically, these defects are associated with a novel role of these proteins in maintaining nuclear pore integrity and the regulation of nucleocytoplasmatic transport. Cyclin Y-CDK16/18 complexes directly phosphorylate the nuclear pore complex (NPC) components NUP35 and NUP214. CDK16/18 inhibition leads to defective nuclear accumulation of the DNA recombinase RAD51, altering DNA repair and inducing lethal levels of DNA damage. Genetic ablation of Cdk16 and Cdk18 in vivo triggers DNA damage and apoptotic cell death in murine liver tumors induced by MYC and -catenin, resulting in tumor regression. Collectively, these data support the development of CDK16/18-targeted therapies for the treatment of HCC.
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 GSE300751_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 PRJNA1282028 and SRA study SRP594535. Searching any of these in the dataset finder brings you back here.

Study design
5 × HCC, CDK18KO, vs 5 × HCC, WT, vs 4 × HCC, CDK16KO CDK18KO,

Supports a between-group comparison across 14 samples.

How we read this: 3 replicated groups read from 14 sample titles; they account for 14 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.