# Metabolomics Analysis of Functional Activity Changes in Residual Tumour Cells After IOCS Treatment

## TL;DR

This study investigates how IOCS treatment affects residual tumor cells in liver cancer patients, finding changes in metabolites and gene activity that suggest improved outcomes.

## Contribution

The study identifies specific metabolomic and molecular changes in residual tumor cells following IOCS treatment in hepatocellular carcinoma.

## Key findings

- Metabolomic analysis revealed six key metabolites differing between IOCS-treated and control groups.
- TP53 expression was significantly upregulated in the experimental group, potentially mediating therapeutic effects.
- IOCS treatment reduced HCC cell migration and apoptosis while altering levels of E2F1, MDM2, TP53, and CTNNB1.

## Abstract

Hepatocellular carcinoma (HCC) is a serious and often lethal cancer, particularly in patients with chronic liver disease. Currently, no specific treatment has been utilised to prevent HCC. The detailed mechanism of HCC is still elusive, and this study aims to identify and characterise the functional activity changes in residual tumour cells following intraoperative cell salvage (IOCS) treatment during HCC surgery. This research is a retrospective case–control study, involving the selection of 60 patients with HCC who underwent radical surgery; then blood and tumour tissue were collected for further testing. GC–MS assay, immunofluorescence, Western blot and qRT‐PCR techniques were employed. Our study found comparable demographic and baseline clinical characteristics between the experimental group (n = 30), which received IOCS treatment during surgery, and the control group (n = 30), which did not receive IOCS treatment, validating subsequent analyses. Metabolomic analysis revealed six key metabolites differing between groups, indicating improvement in liver tumours in the experimental group. TP53 expression was significantly upregulated, potentially mediating therapeutic effects. The intervention reduced HCC cell migration and apoptosis, decreased E2F1 and MDM2 protein and mRNA levels, and increased TP53 and CTNNB1 levels. These findings support the potential clinical application of the intervention in improving treatment outcomes for HCC patients, warranting further investigation to elucidate the underlying mechanisms and optimise therapeutic strategies.