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Disrupting SOX2 Self-Association and Condensates to Overcome Chemotherapeutic Drug Resistance in Lung Squamous Cell Carcinoma [Cut & Run, 2]

GSE314516 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 2 samples Submitted 2026/03/14 Platform GPL29480
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)
Chemotherapy remains one of the most important treatments for lung squamous cell carcinoma (LSCC), yet overcoming chemotherapeutic drug resistance poses a significant challenge. The high frequency of SOX2 copy number amplification observed in LSCC patients underscores its potential role as a regulator in this context. Our investigation reveals a strong correlation between SOX2 amplification and expression levels in LSCC patients.
Read the full summary ↓
Notably, overexpression of SOX2 confers resistance to chemotherapeutic drugs in LSCC cell lines. We elucidate that SOX2 undergoes phase separation, forming condensates that sequester chemotherapeutic agents used in LSCC treatment, thereby exacerbating chemotherapeutic drug resistance in LSCC cells. To address this, we design a small peptide containing 16 amino acids conjugated with 8 arginine, specifically targeting α-helix within HMG domain to disrupt SOX2 self-association. Our data demonstrate that this peptide effectively prevents SOX2 droplet formation, consequently reversing chemotherapy tolerance in LSCC without compromising SOX2 transcriptional activity. Collectively, our findings unveil a novel mechanism of chemotherapy resistance in LSCC mediated by SOX2 phase separation and propose a promising peptide-based therapeutic strategy to combat chemoresistance in LSCC.
This dataset
Open GSE314516 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →
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 GSE314516_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 PRJNA1391444 and SRA study SRP656766. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Samples in this study

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