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LHX2 drives neuroendocrine transformation in TP53/RB1-deficient prostate cancer

GSE328076 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2026/04/16 Platform GPL16791Platform GPL34633
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 14 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)
Topic
Prostate cancerThis series is part of our curated briefing on it.
Samples
14 samples: 14 samples, each with a distinct title — no replicated groupsGroups 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)
Neuroendocrine prostate cancer (NEPC) is an aggressive subtype that progresses after androgen deprivation therapy (ADT) resistance and has extremely poor prognosis. Its underlying regulatory mechanisms remain incompletely understood. Through analyses of cell lines, organoids, transgenic mouse models, and clinical samples, this study systematically revealed the core role and regulatory network of LIM homeobox transcription factor 2 (LHX2) in NEPC occurrence and development.
Read the full summary ↓
In the genetic context of TP53/RB1 deficiency, LHX2 is activated and induces prostate cancer cell transdifferentiation into a neuroendocrine (NE) phenotype. LHX2 and FOXA2 exhibit a mutually exclusive expression pattern, forming two NEPC subpopulations (FOXA2high and LHX2high) that synergistically maintain NE features. Analysis of clinical samples demonstrated that LHX2 expression was closely associated with NEPC progression and ADT resistance. The LHX2-001 transcript containing the LIM domain was found to be the key subtype driving NE transformation, and was found to functionally depend on the transcriptional coactivator CEBPB and to collectively regulate the expression of NE genes. ACTIVIN, identified as a signal specific to the LHX2high subpopulation, played a major role in enhancing tumor stemness, and its key receptor ACVR2B was transcriptionally regulated by LHX2. Targeted blocking of Activin A (garetosmab) effectively inhibited the progression of LHX2-overexpressing tumors. Our findings clarified the molecular mechanism through which specific LHX2 transcripts drive NEPC, revealed the subtype heterogeneity of NEPC, and may provide a new theoretical basis and potential targets for NEPC diagnosis and targeted therapy.
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 GSE328076_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1453808 and SRA study SRP692037. Searching any of these in the dataset finder brings you back here.

Study design
14 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 14 sample titles: 14 distinct titles with little repetition. 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 Prostate cancer datasets

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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.