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Adaptor protein CIN85 potentiates migration of osteosarcoma cells

GSE292011 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/04/14 Platform GPL18573
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
OsteosarcomaThis 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
Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2-COL3A1 axisMolecular oncology · 2026
Summary (written by the submitters)
The adaptor protein CIN85, encoded by the SH3KBP1 gene, is a member of the CIN85/CMS family of adaptor molecules involved in many signaling pathways. CIN85 functionally contributes to different biological processes in normal and cancer cells, such as vesicle-mediated transport, cell adhesion, migration, and invasiveness. In this study, we found that the expression of CIN85 was elevated in osteosarcoma compared to normal bone, and in metastases compared to primary bone tumors.
Read the full summary ↓
Overexpression of CIN85 in osteosarcoma cell lines enhanced their migration and collagen invasion while silencing CIN85 suppressed cell migration. We used human osteosarcoma HOS cells with the overexpression of CIN85 or its knockdown to study the transcriptomic changes induced by this protein. Differentially expressed genes were enriched in cell proliferation, apoptosis, cell differentiation, extracellular matrix, adhesion, focal adhesion, tight junctions, and cell migration. Several abundant signaling pathways involved in tumorigenesis were identified, including NF-κB, TNF, MAPK, Wnt, PI3K/Akt/mTOR, TGF, and VEGF.
Published in
Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2-COL3A1 axis
Horak I, Zambo IS, Přikryl M et al. · Molecular oncology 2026 · PMID 41998852 · doi:10.1002/1878-0261.70245
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 GSE292011_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 PRJNA1236317 and SRA study SRP570492. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 12 more — browse all 12 samples with per-sample file links →

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