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FTO-mediated autophagy inhibition promotes non-small cell lung cancer progression by reducing SESN2 mRNA stability [MeRIP-Seq]

GSE240879 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2024/03/09 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)
Topic
Lung cancerThis series is part of our curated briefing on it.
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
FTO-mediated autophagy inhibition promotes non-small cell lung cancer progression by reducing the stability of SESN2 mRNAHeliyon · 2024
Summary (written by the submitters)
N6-methyladenosine (m6A) serves as the most abundant mRNA modification within eukaryotes that is involved in autophagy and progression of non-small cell lung cancer (NSCLC). The role of the m6A demethylase FTO in NSCLC progression has recently received widespread attention. However, the mechanism of FTO-mediated autophagy regulation in NSCLC progression is unclear.
Read the full summary ↓
In this study, we found that FTO was significantly up-regulated in NSCLC, and down-regulation of FTO blocked the growth, invasion and migration of NSCLC cells via autophagy induction. Importantly, SESN2 was involved in m6A regulation during autophagy in NSCLC cells. FTO deficiency prompted IGF2BP1 to interact with SESN2 mRNA, which led to an increase in SESN2 mRNA stability as well as enhanced SESN2 protein levels. However, FTO inhibited autophagic flux via down-regulation of SESN2, thereby promoting the growth, invasion and migration of NSCLC cells. Our findings uncovered that FTO-mediated autophagy inhibition promotes malignant progression of NSCLC via reduction of SESN2 mRNA stability, thus providing novel notions for the prevention and treatment of NSCLC.
Published in
FTO-mediated autophagy inhibition promotes non-small cell lung cancer progression by reducing the stability of SESN2 mRNA
Wang K, Mei Z, Zheng M et al. · Heliyon 2024 · PMID 38495179 · doi:10.1016/j.heliyon.2024.e27571
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 GSE240879_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 PRJNA1005633 and SRA study SRP455218. Searching any of these in the dataset finder brings you back here.

Samples in this study

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