GEO series

miR-339-5p impairs myogenic proliferation and differentiation by repressing contractile gene programs in skeletal muscle

GSE327356 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2026/06/16 Platform GPL24676Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 18 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: Mus musculus (mouse)
Samples: 18 samples: 18 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)

MicroRNAs (miRNAs) are critical regulators of skeletal muscle development and adaptation, orchestrating the balance between proliferation, differentiation, and tissue repair. Here, we identify miR-339-5p as a previously unrecognized, conserved regulator of skeletal muscle remodeling. Transcriptomic analysis from human, mouse, and rat studies revealed that miR-339-5p is consistently upregulated in skeletal muscle under conditions of stress or injury and declines during myogenic differentiation in vitro.

Read the full summary ↓

Gain-of-function experiments demonstrated that miR-339-5p overexpression impairs expression of genes associated with myogenic differentiation and promotes expression of proliferative markers in both primary human myotubes and mouse C2C12 cells. Transcriptomic profiling confirmed widespread repression of pathways involved in cytoskeletal organization, myofibrillar assembly, and mitochondrial function. In vivo, electroporation-mediated overexpression of miR-339-5p in mouse tibialis anterior altered regeneration-associated gene expression and increased the number of immature fibers, therefore modulating tissue remodeling during post-injury growth. Integrated analyses combining target prediction algorithms, differentiation-associated correlations, and overexpression datasets identified seven conserved high-confidence miR-339-5p targets, among which the autophagy-associated phosphatase MTMR3 emerged as the most consistently regulated candidate. Collectively, our data demonstrate that miR-339-5p functions as a conserved inhibitor of myogenic progression, linking injury-induced stress responses to delayed differentiation and altered muscle remodeling. These findings establish miR-339-5p as a potential therapeutic target in conditions characterized by impaired muscle regeneration or dysregulated tissue remodeling.

This dataset

Open GSE327356 in finder → Find more RNA-seq 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 GSE327356_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 PRJNA1450589 and SRA study SRP690178. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

18 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 18 sample titles: 18 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

GSM9654277 Subject 1 - human cells transfected with negative control miRNA mimic
GSM9654278 Subject 1 - human cells transfected with miR-339 mimic
GSM9654279 Subject 2 - human cells transfected with negative control miRNA mimic
GSM9654280 Subject 2 - human cells transfected with miR-339 mimic
GSM9654281 Subject 3 - human cells transfected with negative control miRNA mimic
GSM9654282 Subject 3 - human cells transfected with miR-339 mimic
GSM9654283 Subject 4 - human cells transfected with negative control miRNA mimic
GSM9654284 Subject 4 - human cells transfected with miR-339 mimic
GSM9654285 Subject 5 - human cells transfected with negative control miRNA mimic
GSM9654286 Subject 5 - human cells transfected with miR-339 mimic
GSM9654287 Subject 6 - human cells transfected with negative control miRNA mimic
GSM9654288 Subject 6 - human cells transfected with miR-339 mimic
GSM9654289 C2C12 n=1, mouse cells transfected with negative control miRNA mimic
GSM9654290 C2C12 n=1, mouse cells transfected with miR-339 mimic
GSM9654291 C2C12 n=2, mouse cells transfected with negative control miRNA mimic
GSM9654292 C2C12 n=2, mouse cells transfected with miR-339 mimic
GSM9654293 C2C12 n=3, mouse cells transfected with negative control miRNA mimic
GSM9654294 C2C12 n=3, mouse cells transfected with miR-339 mimic

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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.