GEO series

Subcellular Trafficking of Oncoprotein FOXK1 Reverses Insulin Resistance-induced Circadian Disruption and Promotes Sensitivity of Metformin in Tumor Therapy

GSE237509 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 2 samples Submitted 2025/07/16 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 2 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Samples: 2 samples
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 pathophysiological function of the FOXK family-member FOXK1 remains to be explored. Although tumors classically induce abnormalities in the insulin pathway, clinical trials have failed to establish insulin receptors as potential targets for tumor therapy. Metformin, so far has been identified as an effective treatment in several clinical oncology trials; however, metformin may fail to benefit all patients, and some even suffer from many side effects and drug resistance.

Read the full summary ↓

Herein, we report that FOXK1 expression correlates with the sensitivity to metformin treatment in a variety of tumors. FOXK1 translocates into the nucleus in response to insulin stimulation and recruits multiple class I HDAC-containing complexes that regulate the expression of genes, such as PER2 and OGT, known to be critically involved in circadian rhythm and insulin resistance. Furthermore, high insulin levels associated with cancer could disturb the subcellular localization and epigenetic regulatory functions of FOXK1. Glycosylation modifications stabilize FOXK1 in the nucleus. Elevated nuclear FOXK1 competes with CLOCK for binding with BMAL1, leading to the deregulation of circadian rhythm, which, in turn, enhanced tumor cell proliferation in vitro and promoted tumor development in vivo. Correspondingly, elevated expression of nuclear FOXK1 was observed during tumor progression and was associated with a poor prognosis. Interestingly, both in vitro and in vivo experiments confirmed that cells with high FOXK1 expression were highly responsive to metformin stimulation. Collectively, these findings revealed that nuclear FOXK1 promotes tumorigenesis by disrupting circadian rhythm under insulin resistance, and its expression may serve as a potential indicator for the adjuvant treatment of tumors using metformin.

This dataset

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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 GSE237509_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA995549 and SRA study SRP449850. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 2 more — browse all 2 samples with per-sample file links →

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