GEO series

RBM25 drives hepatocellular carcinoma progression by regulating oncogenic splicing of MYPT1 and translation of YAP

GSE284351 Homo sapiens (human) RNA-seq (gene expression) 4 samples Submitted 2026/09/21 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 4 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)
Samples: 4 samples
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)

Deregulated splicing factors lead to aberrant alternative splicing (AS), which plays a critical role in tumorigenesis and cancer progression. However, pinpointing the targets and understanding the inherent mechanisms of AS in Hepatocellular Carcinoma (HCC) tumorigenesis remains a complex task. Here, we demonstrate that RNA-binding motif protein 25 (RBM25) is overexpressed in HCC patients, and its elevated expression is associated with worse prognosis.

Read the full summary ↓

Functionally, we confirmed that depletion of RBM25 inhibited HCC progression both in vivo and in vitro. Using RNA-seq, we conducted a comprehensive screening and identified numerous AS events affected by RBM25. Particularly, we found that RBM25 regulates the splicing switch of MYPT1 gene, thereby promoting the expression of the oncogenic isoform MYPT1-L. Consistently, MYPT1-L was overexpressed in HCC patients, and a higher level of MYPT1-L was associated with reduced survival rates. Unexpectedly, further investigation revealed that RBM25 enhances the tumorigenic potential of HCC through regulating Yap translation. In a drug screening targeting RBM25, we discovered that candicidin reduces the level of RBM25 and inhibits HCC growth. Taken together, our study identifies RBM25 as a dual role in modulating MYPT1 splicing and YAP translation to promote HCC progression, representing a potential prognostic biomarker and therapeutic target for HCC.

This dataset

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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 GSE284351_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 PRJNA1198863 and SRA study SRP551704. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42750313) ↗

Samples in this study

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+ 4 more — browse all 4 samples with per-sample file links →

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