Exploring the molecular mechanism of cellular senescence induced by Picrasma quassioides in HepG2 based on RNA...

This study investigates the impact of Picrasma quassioides (PQ) on senescence and proliferation in the human hepatoma cell line HepG2, alongside its potential molecular mechanisms, using RNA sequencing (RNA-seq) in conjunction with in vitro experiments. The study aims to provide a novel theoretical foundation for PQ-based hepatocellular carcinoma (HCC) treatments.

The analysis of chemical components in PQ-containing serum was conducted using UHPLC-Q-Orbitrap HRMS. To assess cell viability, proliferation, and senescence, CCK-8 assays, EdU staining assays, and SA-β-Gal staining assays were performed. Additionally, core differential genes were screened through transcriptome sequencing and network pharmacology. The molecular mechanisms underlying PQ-induced senescence in HepG2 cells were thoroughly elucidated via functional enrichment analysis, construction of protein-protein interaction networks, and molecular docking techniques.

Using UHPLC-Q-Orbitrap HRMS technology, 33 chemical components were identified in PQ. The CCK8 assay demonstrated that PQ exhibited a cytotoxic effect on HepG2 cells, while EdU and SA-β-Gal assays confirmed that PQ could induce cellular senescence and inhibit excessive proliferation. RNA sequencing, in conjunction with network pharmacology, identified 146 key genes, and enrichment analysis revealed that these genes were significantly enriched in the MAPK and PI3K-Akt pathways. Among these, five core targets were identified: MMP2, TGFB1, CXCL8, JUN, and FOS. Molecular docking studies suggested that these core genes could interact with PQ-like compounds.

PQ exerts anti-cancer effects on HCC by inducing cellular senescence, potentially through the MAPK and PI3K-Akt signaling pathways. MMP2, TGFB1, CXCL8, JUN, and FOS may represent key targets of PQ-induced senescence.