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Long non-coding RNA triplex-dependent regulation of melanoma gene networks

GSE302468 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2026/05/26 Platform GPL20301Platform GPL16791
At a glance

RNA-seq (gene expression) · human · 24 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
MelanomaThis series is part of our curated briefing on it.
Samples
24 samples: 6 conditions, mostly in triplicateGroups 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)
SLNCR is a long non-coding RNA that promotes melanoma formation. Previously, we have shown that SLNCR regulates gene expression and melanomagenesis via interacting with different transcription factors. Here we show that SLNCR is associated with several genomic sites that contain RNA: DNA triplex target sites (TTSs). The primary sequence of SLNCR contains 4 triplex forming regions (TFRs), which are homologous to the TFRs of MEG3, HOTAIR, and PARTICLE lncRNAs.
Read the full summary ↓
Full-length SLNCR overexpression promotes proliferation, migration, and invasion of melanoma cells and induces characteristic gene expression changes that are reversed by deletions of TFS-1, -2, -4, or -5. These triplex-dependent genes are enriched in pathways involved in cell cycle regulation and cell migration. We directly demonstrate that SLNCR TFRs can form RNA•DNA-DNA triplexes with the TTSs in promoters of genes, suggesting network level gene regulation. Finally, inhibitory oligos that block SLNCR•DNA-DNA triplex formation reversed the effect of SLNCR-mediated migration and proliferation ex vivo demonstrating that triplex formation might play a role in driving melanoma progression.
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 GSE302468_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 PRJNA1291051 and SRA study SRP601147. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
Empty ×3 SLNCR_Full_Length ×3 SLNCR𝛥TFR1 ×3 SLNCR𝛥TFR2 ×3 SLNCR𝛥TFR4 ×3 SLNCR𝛥TFR5 ×3 Empty_Rep1 ×1 Empty_Rep2 ×1 +4 more

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 24 sample titles; they account for 18 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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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.