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Effect of pharmacological inhibition of SMYD3 on gene expression in patient-derived CRC-SCs

GSE264227 Homo sapiens (human) RNA-seq (gene expression) 42 samples Submitted 2025/06/17 Platform GPL18573
At a glance

RNA-seq (gene expression) · human · 42 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
Colorectal cancerThis series is part of our curated briefing on it.
Samples
42 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.
Paper
Tailoring a novel colorectal cancer stem cell-targeted therapy by inhibiting the SMYD3/c-MYC axisSignal transduction and targeted therapy · 2025
Summary (written by the submitters)
Cancer stem cells (CSC) are responsible for colorectal cancer (CRC) chemoresistance, recurrence, and metastasis. Therefore, it has become crucial finding critical molecular stemness targets that are essential for tumor growth. Here, we performed an extensive in vitro and in vivo molecular and functional characterization revealing the pivotal role of SMYD3 in CSC biology.
Read the full summary ↓
Specifically, SMYD3 interacts with and methylates c-MYC at K158 and K163, modulating its transcriptional activity implicated in stemness and colorectal malignancy. Together, all the in vitro data collected, suggest that SMYD3 pharmacological inhibition affects clonogenic and self-renewal potential of patient-derived CRC-SCs and organoids by altering their molecular signature. Moreover, we showed that SMYD3 stable knock-out or its pharmacological inhibition drastically reduced CRC tumorigenicity in vivo, and reduced the metastatic potential of CRC-SCs. Thus, our findings identify SMYD3 as a promising therapeutic target, acting directly on c-MYC, with potential implications for countering CRC-SCs proliferation, chemoresistance, and metastatic dissemination.
Published in
Tailoring a novel colorectal cancer stem cell-targeted therapy by inhibiting the SMYD3/c-MYC axis
Lepore Signorile M, Di Nicola E, Forte G et al. · Signal transduction and targeted therapy 2025 · PMID 40588481 · doi:10.1038/s41392-025-02290-z
This dataset
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.

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 GSE264227_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1101506 and SRA study SRP502415. Searching any of these in the dataset finder brings you back here.

Samples in this study

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