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CDK4 maintains cytoskeletal homeostasis by restraining actomyosin contractility

GSE336354 Homo sapiens (human) RNA-seq (gene expression) 8 samples Submitted 2026/06/28 Platform GPL34295
At a glance

RNA-seq (gene expression) · human · 8 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
Breast cancerThis series is part of our curated briefing on it.
Samples
8 samples: 4 × WT vs 4 × KOGroups 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)
Cyclin-dependent kinase 4 (CDK4) is best known for its canonical role in cell-cycle control, yet how CDK4 activity intersects with cellular architecture remains poorly defined. Here, we uncover a non-canonical function of CDK4 in maintaining cytoskeletal mechanical homeostasis in triple-negative breast cancer (TNBC) cells. We show that CDK4 phosphorylates the RhoA-targeting RhoGAP Myo9b at serine 1935, enhancing its GAP activity and restraining RhoA–ROCK–pMLC-dependent actomyosin contractility.
Read the full summary ↓
Loss or inhibition of CDK4 alters cell morphology, disrupts actin organization, and increases contractility. Elevated contractility in CDK4-deficient cells induces collapse of the intermediate filament network, characterized by Vimentin reorganization and mitochondrial redistribution, indicating a higher-order defect in cytoskeletal architecture. Furthermore, CDK4 expression negatively correlates with pMLC levels in both mouse TNBC tumors and human breast cancer samples, supporting the physiological relevance of this pathway. Together, these findings identify CDK4 as a regulator of cellular mechanical stability, integrating actin dynamics, intermediate filament integrity, and organelle positioning, and reveal an unexpected role for CDK4 beyond cell-cycle regulation.
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 GSE336354_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 PRJNA1481322 and SRA study SRP712051. Searching any of these in the dataset finder brings you back here.

Study design
4 × WT vs 4 × KO

Supports a between-group comparison across 8 samples.

How we read this: 2 replicated groups read from 8 sample titles; they account for 8 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 Breast cancer datasets

Search all human RNA-seq datasets in GEO →

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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.