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Depression and Anxiety-Induced Metabolic Reprogramming Promotes Hepatocellular Carcinoma Progression through CBX5 Lactylation: Involvement of Taurocholate and PHGDH-Mediated Ferroptosis

GSE282171 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 28 samples Submitted 2025/12/01 Platform GPL19057Platform GPL24676Platform GPL13112Platform GPL11154
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 28 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Mus musculus (mouse)
Topic
Hepatocellular carcinomaThis series is part of our curated briefing on it.
Samples
28 samples: 19 distinct titles, 3 of them repeatedGroups 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)
Traditional Chinese medicine posits that emotional disorders like depression and anxiety can lead to liver qi stagnation, promoting the occurrence and progression of hepatocellular carcinoma (HCC). However, the specific mechanisms remain unclear. This study investigated the association between depression and HCC risk through large-scale epidemiological analyses, and the underlying biological mechanisms were explored.
Read the full summary ↓
Data were analyzed from the China Health and Retirement Longitudinal Study (CHARLS; n = 14,770) and the National Health and Nutrition Examination Survey (NHANES; n = 29,983), assessing depression levels and HCC risk. Participants with moderate to severe depression had a significantly increased risk of HCC compared to those without depression in both CHARLS (adjusted hazard ratio [HR] = 2.27; 95% confidence interval [CI]: 1.05–4.91) and NHANES (adjusted odds ratio [OR] = 5.96; 95% CI: 2.42–14.04). A meta-analysis indicated an overall 3.59-fold increased risk of HCC (95% CI: 1.40–9.24) among depressed participants. These findings remained robust across sensitivity analyses. Building on these results, a social isolation (SI) model was employed to study the impact of depression on HCC progression. SI significantly accelerated HCC progression in a spontaneous tumor mouse model. Mechanistically, social isolation drove metabolic reprogramming in HCC, characterized by elevated lactate levels, which in turn led to increased protein expression and lactylation of one of the key transcriptional regulators, CBX5. Knockout of Cbx5 attenuated the progression of HCC associated with social isolation in the transgenic mouse model. Then, it was shown that lactylation of CBX5 at the K91 site enhances its nuclear translocation, promoting tumor proliferation through enhancing the accumulation of taurocholate and upregulating PHGDH via forming a complex with c-Myc to inhibit ferroptosis. The elevated taurocholate disrupted the interaction between RNF123 and CBX5, stabilizing CBX5 in HCC. To target this pathway, a novel H-PROTAC molecule was developed that effectively degrades CBX5, enhances ferroptosis, and inhibits HCC proliferation, demonstrating potential therapeutic value. In conclusion, the study reveals the critical role of depression and anxiety-induced CBX5 lactylation in HCC occurrence and progression within a social isolation model. These findings provide new insights into HCC prevention and treatment, suggesting that CBX5-targeted therapies hold significant potential for HCC treatment.
This dataset
Open GSE282171 in finder → Find more RNA-seq datasets → Hepatocellular carcinoma 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 GSE282171_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1187514 and SRA study SRP545916. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
19 distinct titles, 3 of them repeated
CR-Mlg ×6 CBX5-Si ×3 CBX5-NC ×3

How we read this: Read from 28 sample titles: 19 distinct titles with little repetition. 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 Hepatocellular carcinoma datasets

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