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LIN28B-mediated activation of the PI3K/AKT pathway promotes metastasis and unravels a new therapeutic vulnerability in colorectal cancer

GSE269369 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2025/06/07 Platform GPL20301
At a glance

RNA-seq (gene expression) · human · 18 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
Colorectal cancerThis series is part of our curated briefing on it.
Samples
18 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)
Colorectal cancer (CRC) remains a leading cause of cancer death, primarily due to metastatic spread. LIN28B, an RNA-binding protein overexpressed in 30% of CRCs, acts as an oncogene and promotes CRC metastasis. However, the mechanisms through which LIN28B drives these effects remain unclear. In this study, we genetically modified CRC cell lines to overexpress LIN28B, leading to enhanced activation of the PI3K/AKT pathway and increased metastatic potential in mice.
Read the full summary ↓
We developed genetically engineered mouse models (GEMMs) with mutant PIK3CA that are the first to exhibit primary intestinal tumors progressing to liver metastases with an intact immune system. Pharmacological inhibition with the PI3Kα-specific inhibitor alpelisib effectively reduced migration and invasion in vitro, as well as metastasis in vivo. Treatment of CRC patient-derived organoids (PDOs) with alpelisib, the AKT inhibitor capivasertib, and/or the S6K inhibitor LY2584702 demonstrated the potential of pathway inhibition to impair tumor growth. Tissue microarrays from CRC patients further indicated that pathway activation correlates with disease progression. These findings underscore the critical role of the PI3K/AKT pathway in CRC metastasis and open new avenues in targeted inhibition and combination therapies in metastatic CRC (mCRC).
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 GSE269369_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 PRJNA1121279 and SRA study SRP512459. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
LoVo_EV ×3 LoVo_LIN28B ×3 LoVo_LIN28B_Alp ×3 DLD1_EV ×3 DLD1_LIN28B ×3 DLD1_LIN28B_Alp ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 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.