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HMGB3 promotes brain metastasis in lung adenocarcinoma by recruiting SSBP1 for nuclear translocation to remodel mitochondrial metabolism

GSE293936 Homo sapiens (human) Single-cell RNA-seq 12 samples Submitted 2025/12/31 Platform GPL24676
At a glance

Single-cell RNA-seq · human · 12 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Homo sapiens (human)
Topic
Lung cancerThis series is part of our curated briefing on it.
Samples
12 samples: 3 × H2030 cells, biol vs 3 × H2030-Lbrm cells, biol vs 3 × H2030-Lbrm-NC cells, biol vs 3 × H2030-Lbrm-siHMGB3 cells, biolGroups 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.
Paper
HMGB3 promotes brain metastasis of lung adenocarcinoma by recruiting SSBP1 for nuclear translocation to remodel mitochondrial metabolismCancer communications (London, England) · 2025
Summary (written by the submitters)
Background: Brain metastasis, a leading cause of death in patients with lung adenocarcinoma (LUAD), arises from tumor cells adapting to the brain’s unique microenvironment of the brain through metabolic remodeling regulated by key oncogenes. Here, we aimed to determine the role of high mobility group protein B3 (HMGB3) in regulating tumor cell metabolism to promote the progression and brain metastasis in LUAD.
Read the full summary ↓
Methods: In this study, a LUAD cell model predisposed to brain metastasis was developed in this study, and differentially expressed genes HMGB3 was identified. HMGB3 expression in LUAD was then validated through a series of in vitro and in vivo experiments, including western blotting, single-cell RNA sequencing (scRNA-seq), and immunohistochemistry (IHC). Tissue microarray (TMA) and LUAD brain metastasis clinical samples were used to explore the expression of HMGB3 and its clinical significance in LUAD. Additionally, we performed gene enrichment analysis on scRNA-seq and bulk RNA-seq, along with western blotting, to identify the pathways through which HMGB3 may cause brain metastasis. We then used coimmunoprecipitation and mass spectrometry to identify protein single-stranded DNA binding protein 1 (SSBP1), which interacts with HMGB3. Finally, gain and loss-of-function and rescue experiments were conducted to study SSBP1’s roles in LUAD cells. Results: HMGB3 upregulation in LUAD primary tumors and brain metastases associated with poor prognosis independent of metastasis. HMGB3 enhanced the migration, invasion, and epithelial-mesenchymal transition (EMT) capabilities of LUAD cells in vitro and promotes the occurrence and development of brain metastasis in vivo. Mechanistically, HMGB3 recruited SSBP1, inducing its nuclear translocation and reprogramming mitochondrial metabolism, thereby increasing cytoplasmic reactive oxygen species (ROS) levels, which activated the phosphatidylinositol 3-kinase–protein kinase B (PI3K-Akt) pathway by downregulating phosphatase and tensin homolog (PTEN), enhancing tumor cell proliferation, migration, invasion, and EMT. Conclusions: This study demonstrated that HMGB3 functions as a driver gene in the brain metastasis of LUAD, promoting metabolic adaptation of tumor cells to the brain microenvironment through the regulation of mitochondrial metabolism, thereby offering potential therapeutic targets for LUAD brain metastases.
Published in
HMGB3 promotes brain metastasis of lung adenocarcinoma by recruiting SSBP1 for nuclear translocation to remodel mitochondrial metabolism
Cui H, Yang Y, Li S et al. · Cancer communications (London, England) 2025 · PMID 41194553 · doi:10.1002/cac2.70075
This dataset
Open GSE293936 in finder → Find more human RNA-seq datasets → Lung cancer landscape →
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.

Series matrix ↓
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 GSE293936_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

What the files usually look like: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1247466 and SRA study SRP577046. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41194553) ↗
Study design
3 × H2030 cells, biol vs 3 × H2030-Lbrm cells, biol vs 3 × H2030-Lbrm-NC cells, biol vs 3 × H2030-Lbrm-siHMGB3 cells, biol

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
More Lung cancer datasets

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