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Epigenetic silencing and CRISPR-mediated reactivation of Tight Junction Protein Claudin 10 B (CLDN10B) in Skin Cancer.

GSE283785 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/06/25 Platform GPL24676
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: 3 × HEK EGFP uninduced vs 3 × HEK EGFP induced vs 3 × HEK CLDN10B-EYFP uninduced vs 3 × HEK CLDN10B-EYFP inducedGroups 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.
Paper
Epigenetic silencing and CRISPR-mediated reactivation of tight junction protein claudin10b (CLDN10B) in renal cancerClinical epigenetics · 2025
Summary (written by the submitters)
The kidney's tubular system relies on cell polarity and tight junctions to maintain structure and function and disruptions contribute to diseases like cancer. Loss of tight junction proteins such as Claudins, can actively contribute to tumorigenesis. We aimed to identify biomarkers for renal carcinoma, after kidney transplantation and conventional kidney tumors.
Read the full summary ↓
We identified the epigenetic silencing of the Claudin 10 gene isoform B (CLDN10B) through DNA hypermethylation in renal cancers, including clear cell- (ccRCC), papillary - (pRCC) and post-transplantation renal carcinoma (PT-RCC). In contrast, CLDN10A, was hypomethylated in ccRCC and pRCC. Differential methylation of the Isoforms discriminates RCC from other malignancies. The epigenetic alteration of CLDN10B significantly correlated with reduced patient survival and advanced tumor staging. CLDN10B overexpression or induction significantly inhibited migration, cell cycle progression, and cellular growth. Using a CRISPR-based epigenetic editing reactivated CLDN10B to its endogenous level using VP160 and TET1 by promoter demethylation and significantly demonstrated its tumor-suppressive effects in 2D and 3D cell models. Our findings suggest that CLDN10B acts as a tumor suppressor, and its epigenetic regulation may represent a therapeutic target for RCC. Ultimately, understanding CLDN10B’s regulation and function could provide new insights into renal cancer treatment.
Published in
Epigenetic silencing and CRISPR-mediated reactivation of tight junction protein claudin10b (CLDN10B) in renal cancer
Arroyo Villora S, Zhao Y, Castellanos Silva P et al. · Clinical epigenetics 2025 · PMID 40524239 · doi:10.1186/s13148-025-01911-2
This dataset
Open GSE283785 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 GSE283785_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 PRJNA1195583 and SRA study SRP550059. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40524239) ↗
Study design
3 × HEK EGFP uninduced vs 3 × HEK EGFP induced vs 3 × HEK CLDN10B-EYFP uninduced vs 3 × HEK CLDN10B-EYFP induced

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
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