GEO series

Effect of stable genetic ablation and pharmacological inhibition of SMYD3 on gene expression in CRC cell line (HCT-116)

GSE264157 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/06/17 Platform GPL18573

At a glance

RNA-seq (gene expression) · human · 12 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: 12 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

Open GSE264157 in finder → Find more human 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 GSE264157_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 PRJNA1101069 and SRA study SRP502109. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40588481) ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 12 more — browse all 12 samples with per-sample file links →

Datasets on a similar topic

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GSE289011 Genetic or pharmacological inactivation of CREBBP sensitizes B-cell Acute Lymphoblastic Leukemia to Ferroptotic Cell Death upon BCL2 Inhibition [ChIP-seq] 4 samples shares pharmacological, inhibition, genetic
GSE265926 Epigenetic and oncogenic inhibitors cooperatively drive differentiation and kill KRAS-mutant colorectal cancers [CRC cell lines] 48 samples shares crc, genetic
GSE36895 Molecular Genetic Classification of clear-cell Renal Cell Carcinoma (ccRCC) based on the Gene Expression Profiling of Tumors and Tumorgrafts deficient for BAP1 or PBRM1 76 samples shares crc, genetic
GSE254366 Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. 36 samples shares crc, inhibition
GSE254365 Epigenome reprogramming through H3K27 and H3K4 trimethylation as a resistance mechanism to DNA methylation inhibition in BRAFV600E-mutated CRC. [ChIP-Seq] 30 samples shares crc, inhibition

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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.