← BioTransfer GEO Dataset Finder
GEO series

Restoring Taxane Efficacy in Castration Resistant Prostate Cancer Through Targeting Menin

GSE302154 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 20 samples Submitted 2025/07/31 Platform GPL28038Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 20 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
20 samples: 6 conditions, mostly in triplicateGroups 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.
Paper
Menin-driven mTOR signaling sustains taxane resistance in CRPC and reveals a targetable vulnerability for combination therapyCell communication and signaling : CCS · 2025
Summary (written by the submitters)
Prostate cancer (PC) typically depends on hormones for growth, with androgen deprivation therapy (ADT) serving as the primary treatment. However, many patients progress to a castration-resistant (CR) stage, where their tumor becomes unresponsive to ADT. Despite the common use of conventional chemotherapeutics like taxanes (docetaxel, cabazitaxel), the majority of patients experience recurrence.
Read the full summary ↓
To uncover the mechanisms underlying the drug-resistant phenotype, we developed docetaxel-resistant CRPC cell lines, and through a drug library screen, we identified MLL-Menin and MLL-WDR5 inhibitors that overcome taxane resistance and significantly induced G2/M arrest and apoptosis. To determine the roles of individual proteins in the MLL complexes, we silenced several MLL partner proteins , and the absence of Menin and LEDGF particularly halted the growth of the resistant cells while showing no significant effect on parentals. Notably, parental cells with Menin silencing failed to develop resistance even after prolonged exposure, unlike their Menin-expressing counterparts, highlighting the critical role of Menin in the resistance process. Menin knockouts were analyzed through RNA-sequencing, and several gene sets, including E2F targets, G2/M checkpoints, and mTORC1 pathways, were found to be negatively regulated in taxane-resistant cells. The ablation of Menin led to a reduction in mTOR levels, and ChIP-qPCR analysis confirmed that Menin was enriched on the mTOR promoter. According to TCGA clinical data, the correlation between MEN1 and mTOR became stronger as the disease advanced to metastatic stages. Furthermore, the combination of the mTOR inhibitor Torin1 and docetaxel enhanced the sensitivity of our resistant cells. Menin deficiency reduced cell proliferation and key expression of cell cycle genes (Cyclin D1, CDK20). Rescue experiments reversed these effects, and Menin showed significant enrichment of the Cyclin D1 and CDK20 promoters. Finally, Menin loss impaired docetaxel resistant CRPC growth in our in vivo model. Our data demonstrate the essentiality of Menin for docetaxel resistance and suggest a combined approach targeting both Menin and mTOR to improve taxane therapy responses. Additionally, Menin regulates some key cell cycle genes to promote the G1/S transition, emphasizing its critical role in cell cycle regulation and the growth of taxane-resistant CRPC.
Published in
Menin-driven mTOR signaling sustains taxane resistance in CRPC and reveals a targetable vulnerability for combination therapy
Bulut I, Cevatemre B, Yuksel-Catal N et al. · Cell communication and signaling : CCS 2025 · PMID 41413907 · doi:10.1186/s12964-025-02594-1
This dataset
Open GSE302154 in finder → Find more human RNA-seq datasets → Prostate cancer landscape →
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 GSE302154_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 PRJNA1289086 and SRA study SRP607468. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41413907) ↗
Study design
6 conditions, mostly in triplicate
Du145-P, Non-targeting guide, Replica # ×3 Du145-P, MeninKnockout2, Replica # ×3 Du145-P, MeninKnockout3, Replica # ×3 Du145-DtxR, Non-targeting guide, Replica # ×3 Du145-DtxR, MeninKnockout2, Replica # ×3 Du145-DtxR, MeninKnockout3, Replica # ×3 Du145-DtxR, Menın-IGG-control ×1 Du145-DtxR, Menin-FLAG ×1

Supports a case/control comparison: 12 samples read as cases, 7 as controls.

How we read this: 6 replicated groups read from 20 sample titles; they account for 18 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 Prostate cancer datasets

Search all human RNA-seq datasets in GEO →

Share this dataset

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.