GEO series

Hypoxic stabilization of RIPOR3 mRNA via METTL3-mediated m6A RNA methylation drives breast tumor growth and metastasis [RNA-seq]

GSE263916 Homo sapiens (human) DNA methylation 12 samples Submitted 2026/04/30 Platform GPL29480

At a glance

DNA methylation · human · 12 samples

What it is: DNA methylationChemical marks on DNA that help switch genes on or off.
Organism: Homo sapiens (human)
Topic: Breast cancerThis series is part of our curated briefing on it.
Samples: 12 samples: 3 × MDA-MB-231, N, shControl, vs 3 × MDA-MB-231, N, shRIPOR3, vs 3 × MDA-MB-231, H, shControl, vs 3 × MDA-MB-231, H, shRIPOR3,Groups 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)

N6-methyladenosine (m6A) modification is the most abundant internal mRNA modification in eukaryotes. Hypoxia induces reprogramming of m6A epitranscriptome, but the detail underlying regulator mechanism remains elusive in breast cancer. Here we reported that hypoxia induced elevated m6A modification involved in tumor progression. m6A- sequencing (m6A-seq) combined with RNA sequencing (RNA-seq) identified RIPOR3 as a key target gene of m6A modification under hypoxic stress.

Read the full summary ↓

Hypoxia-induced increased of RIPOR3 m6A levels promoted its mRNA stability and expression, thereby facilitating the progression and metastasis of breast cancer. Besides, RIPOR3 was overexpressed in breast cancer cells and breast tumor tissues, and elevation of RIPOR3 expression was associated with poor prognosis. Mechanistically, RIPOR3 bound to EGFR and the interaction was enhanced under hypoxia, promoting the activation of the EGFR downstream PI3K-AKT signaling pathway. Altogether, our studies reveal that RIPOR3 responds to hypoxic stress to promote EGFR-PI3K-AKT signal pathway, facilitating breast cancer progression and metastasis, thus presenting itself as a potential therapeutic target.

This dataset

Open GSE263916 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 GSE263916_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 beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1099913 and SRA study SRP501621. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

3 × MDA-MB-231, N, shControl, vs 3 × MDA-MB-231, N, shRIPOR3, vs 3 × MDA-MB-231, H, shControl, vs 3 × MDA-MB-231, H, shRIPOR3,

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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

GSM8207463 MDA-MB-231, N, shControl, rep1 MDA-MB-231, N, shContr…
GSM8207464 MDA-MB-231, N, shControl, rep2 MDA-MB-231, N, shContr…
GSM8207465 MDA-MB-231, N, shControl, rep3 MDA-MB-231, N, shContr…
GSM8207466 MDA-MB-231, N, shRIPOR3, rep1 MDA-MB-231, N, shRIPOR…
GSM8207467 MDA-MB-231, N, shRIPOR3, rep2 MDA-MB-231, N, shRIPOR…
GSM8207468 MDA-MB-231, N, shRIPOR3, rep3 MDA-MB-231, N, shRIPOR…
GSM8207469 MDA-MB-231, H, shControl, rep1 MDA-MB-231, H, shContr…
GSM8207470 MDA-MB-231, H, shControl, rep2 MDA-MB-231, H, shContr…
GSM8207471 MDA-MB-231, H, shControl, rep3 MDA-MB-231, H, shContr…
GSM8207472 MDA-MB-231, H, shRIPOR3, rep1 MDA-MB-231, H, shRIPOR…
GSM8207473 MDA-MB-231, H, shRIPOR3, rep2 MDA-MB-231, H, shRIPOR…
GSM8207474 MDA-MB-231, H, shRIPOR3, rep3 MDA-MB-231, H, shRIPOR…

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
GSE271704 5G-exposed human skin cells do not respond with altered gene expression and methylation profiles [RNA-Seq] 120 samples shares methylation, rna-seq
GSE274999 Clinical response to azacitidine in MDS is associated with distinct DNA methylation changes in HSPCs [RNA-Seq] 52 samples shares methylation, rna-seq
GSE284289 Removal of promoter DNA methylation by epigenome editing reverses HBG silencing [RNA-seq] 40 samples shares methylation, rna-seq

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