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Effect of depletion of CYP4F11 on proliferation and migration in lung cancer cell lines NCI-H460 cell line.

GSE310024 Homo sapiens (human) RNA-seq (gene expression) 2 samples Submitted 2026/02/11 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 2 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
Lung cancerThis series is part of our curated briefing on it.
Samples
2 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
On the interface of fatty acid metabolism: A crosstalk between fatty acid ω-hydroxylase CYP4F11 and fatty acid desaturase 2 in non-small cell lung cancerDrug metabolism and disposition: the biological fate of chemicals · 2026
Summary (written by the submitters)
Lung cancer remains the leading cause of cancer deaths worldwide. Drug resistance in lung cancer patients often limits treatment effectiveness, underscoring the need for novel therapeutic targets. In our recent work, we identified the cytochrome P450 4F11 (CYP4F11) as a promising therapeutic target for lung cancer. CYP4F11 belongs to the CYP4F family of fatty acid omega-hydroxylases catalyzing the conversion of arachidonic acid to the potent lipid mediator 20-hydroxyeicosatetraenoic acid (20-HETE).
Read the full summary ↓
20-HETE is a long-known key player in cancer cell proliferation and migration. CYP4F11 is highly overexpressed in patients with lung cancer. Through genetic modification studies in lung cancer cell lines, we found that CYP4F11 indeed mediates the proliferation and migration through 20-HETE production. However, it is currently unknown how CYP4F11 contributes to lung cancer progression and what the underlying mechanism is. Our data identify differentially expressed genes in CYP4F11-knockdown lung cancer cells compared to control cells via RNA sequencing. We provide better understanding on the cellular mechanism involving CYP4F11 in lung cancer.
Published in
On the interface of fatty acid metabolism: A crosstalk between fatty acid ω-hydroxylase CYP4F11 and fatty acid desaturase 2 in non-small cell lung cancer
Jia H, Brixius-Anderko S · Drug metabolism and disposition: the biological fate of chemicals 2026 · PMID 41500153 · doi:10.1016/j.dmd.2025.100221
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 GSE310024_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 PRJNA1365026 and SRA study SRP644899. Searching any of these in the dataset finder brings you back here.

Samples in this study

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