Clinical and Translational Medicine

• Primary synthesis and metabolic routes of peripheral 5-hydroxytryptamine in the gastrointestinal tract.
• Advanced research has established a strong association between the serotonergic components and carcinogenic mechanisms.
• The interplay between serotonergic signalling and the immune system within the tumour microenvironment orchestrates antitumour immune responses.
• Serotonergic-targeted drugs offer valuable clinical options for cancer therapy.

• Lactylation significantly influences tumour metabolism and gene regulation, contributing to cancer progression.

• Advanced sequencing and machine learning reveal widespread lactylation sites in tumours.

• Targeting lactylation enzymes shows promise in enhancing anti-tumour drug efficacy and overcoming chemotherapy resistance.

• This review outlines the clinical implications and future research directions of lactylation in oncology.

1. PUS7 and ALKBH3 are characterized as novel tumour suppressors in gastric cancer.

2. PUS7 enhances the translation efficiency of ALKBH3 through its pseudouridylation activity on ALKBH3 mRNA, thereby inhibiting gastric tumourigenesis.

3. The expression levels of PUS7 and ALKBH3 are significantly correlated in gastric tumours, which may be potential prognostic predictors and therapeutic targets for patients with gastric cancer.

• The source of mesenchymal stem cells (MSCs) strongly influences the composition and function of MSC-derived extracellular vesicles (EVs), affecting their therapeutic potential. Adipose-derived MSC-EVs, known for their immunoregulatory properties and ease of isolation, show promise as a treatment for inflammatory bowel disease (IBD).
• MicroRNAs are consistently present in MSC-EVs across cell types and are involved in pathways that are dysregulated in IBD, making them potential therapeutic agents. For example, miR-let-7a is associated with inhibition of apoptosis, miR-100 supports cell survival, miR-125b helps suppress pro-inflammatory cytokines and miR-20 promotes anti-inflammatory M2 macrophage polarisation.
• Preclinical studies in IBD models have shown that MSC-EVs reduce intestinal inflammation by suppressing pro-inflammatory mediators (e.g., TNF-α, IL-1β, IL-6) and increasing anti-inflammatory factors (e.g., IL-4, IL-10). They also promote mucosal healing and strengthen the integrity of the gut barrier, suggesting their potential to address IBD pathology.