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Site-Specific HPV18 Integration Facilitates Cervical Carcinogenesis through metabolic reprogramming-Induced dysfunction of the SpHK1/S1P/S1PR1 pathway

GSE285710 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2025/08/06 Platform GPL24676
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)
Samples
24 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)
The integration of high-risk human papillomavirus (HR-HPV) into specific loci of the human genome is a pivotal event in cervical carcinogenesis. However, how HPV integration contributes to malignant transformation remains unclear. Here, we utilized the CRISPR/Cas9 system established an 8q24 site-specific HPV18 gene knock-in cell model.
Read the full summary ↓
We discovered that HPV18 knock-in resulted in a global alteration of the genome's topologically associating domain (TAD) structure and up-regulation of cancer-related genes in HaCaT cells, leading to malignant transformation. Furthermore, the IL-17 signaling pathway and S100A8/A9 genes were found to be significantly up-regulated in the HPV18 knock-in cell line, as well as K14-HPV transgenic mice and cervical cancer clinical database. Metabolic reprogramming of the HPV18 knock-in cell line, particularly the up-regulation of glycolysis, facilitated glycerolipid synthesis and Sphingosine-1-phospate(S1P) secretion. The increased secretion of S1P and activation of the S1P receptor 1(S1PR1) signaling pathway induced the expression of S100A8/A9 and cytokines. Inhibition of the S1P/S1PR1 signaling pathway down-regulated the expression of S100A8/A9 and suppressed the growth of HPV18 knock-in cell line and cervical cancer patient derived Xenograft. These findings provide novel insights into the molecular mechanisms underlying cervical carcinogenesis and identify potential therapeutic targets for its treatment.
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 GSE285710_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 PRJNA1205690 and SRA study SRP554934. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 24 more — browse all 24 samples with per-sample file links →

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