GEO series

Transcriptomic profiling of MCF7 ESR1 Y537S mutant cells treated with abemaciclib and/or fulvestrant

GSE336734 Homo sapiens (human) RNA-seq (gene expression) 8 samples Submitted 2026/06/29 Platform GPL30173

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: 2 × MCF7_ESR1_DMSO vs 2 × MCF7_ESR1_LY vs 2 × MCF7_ESR1_Fulv vs 2 × MCF7_ESR1_LYFulvGroups 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)

The retinoblastoma protein (Rb) is a tumour suppressor best known for repressing E2F transcription factors and halting cell cycle progression. In hormone receptor-positive (HR+) breast cancer, CDK4/6 inhibitors activate Rb by preventing its phosphorylation, forming a key component of current endocrine therapy regimens. How pharmacologically activated Rb remodels chromatin and influences transcription beyond cell cycle arrest remains poorly understood.

Read the full summary ↓

Here we show that CDK4/6 inhibition induces redistribution of hypo-phosphorylated Rb to promoters and enhancers. While Rb predictably binds to cell cycle gene promoters to repress transcription, at other sites it unexpectedly promotes expression of oestrogen-responsive genes by integrating into oestrogen receptor (ER)-rich transcriptional hubs. CDK4/6 inhibition enhances ER target gene expression in breast cancer cells, patient-derived xenografts, and clinical HR+ breast cancer samples in an Rb-dependent manner. This reprogramming is mediated in part by KDM5A, whose interaction with Rb contributes to gene regulation at these loci. Critically, components of this Rb-driven ER transcriptional program are pro-proliferative. In endocrine-sensitive tumours, this can be neutralised with anti-oestrogen therapy, explaining therapeutic synergy. In endocrine-resistant settings such as ESR1-mutant breast cancer, the program persists, limiting therapeutic efficacy. These findings reframe Rb as a dual-function transcriptional regulator that, while enforcing cell cycle arrest, can also activate programs that counteract its tumour suppressor function.

This dataset

Open GSE336734 in finder → Find more human RNA-seq datasets → Breast 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 GSE336734_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: 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 PRJNA1482483 and SRA study SRP712926. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

2 × MCF7_ESR1_DMSO vs 2 × MCF7_ESR1_LY vs 2 × MCF7_ESR1_Fulv vs 2 × MCF7_ESR1_LYFulv

Supports a between-group comparison across 8 samples.

How we read this: 4 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

GSM9841526 MCF7_ESR1_DMSO_rep1 MCF7_ESR1_DMSO
GSM9841527 MCF7_ESR1_DMSO_rep2 MCF7_ESR1_DMSO
GSM9841528 MCF7_ESR1_LY_rep1 MCF7_ESR1_LY
GSM9841529 MCF7_ESR1_LY_rep2 MCF7_ESR1_LY
GSM9841530 MCF7_ESR1_Fulv_rep1 MCF7_ESR1_Fulv
GSM9841531 MCF7_ESR1_Fulv_rep2 MCF7_ESR1_Fulv
GSM9841532 MCF7_ESR1_LYFulv_rep1 MCF7_ESR1_LYFulv
GSM9841533 MCF7_ESR1_LYFulv_rep2 MCF7_ESR1_LYFulv

More Breast cancer datasets

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GSE104675 Role for the Transcriptional Activator ZRF1 in Breast Cancer Progression and Endocrine Resistance 6 samples same disease briefing
GSE10885 An integromic analysis reveals that metaplastic carcinomas are distinct from basal-like tumors. 244 samples same disease briefing
GSE10886 A Supervised Risk Predictor of Breast Cancer Based on Biological Subtypes 226 samples same disease briefing
GSE11121 The humoral immune system has a key prognostic impact in node-negative breast cancer 200 samples same disease briefing
GSE336731 Transcriptomic profiling of MCF7 ESR1-PARENT and ESR1-Y537S cells cultured under estrogen-depleted or estradiol-supplemented conditions following abemaciclib treatment and CCND1 knockdown 36 samples shares y537s, mcf7, esr1, abemaciclib
GSE314294 MCF-7 cells long-term treated with Fulv plus Abema acquired ESR1 Y537S mutation and exhibited defective RSR and DDR 9 samples shares y537s, esr1, treated
GSE51448 Gene expression analysis of estrogen receptor mutants, S463P, Y537S and D538G in MCF7 cells 36 samples shares y537s, mcf7, mutant

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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.