J Biochem Mol Toxicol. 2026 Jul;40(7):e71018. doi: 10.1002/jbt.71018.
ABSTRACT
This study aimed to investigate the biological effects of Picroside II on colorectal cancer (CRC) cells, including its impacts on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), and to explore whether its mechanism of action involves modulation of the Notch1 signaling pathway. Human CRC cell lines SW480 and SW620 were treated with various concentrations of Picroside II (10-100 μM). Cell proliferation was assessed using the CCK-8 assay, colony formation assay, and EdU incorporation assay. Migration and invasion capacities were evaluated by wound healing and Transwell assays. The expression levels of EMT-related markers (E-cadherin, N-cadherin, Vimentin, ZEB2) and key proteins in the Notch1 pathway (Notch1, Cleaved Notch1, RBP, HES1) were analyzed by Western blotting. Statistical analysis was performed using one-way ANOVA and Student’s t-test. Picroside II inhibited the proliferation of SW480 and SW620 cells in a dose- and time-dependent manner, reduced colony formation ability, and decreased DNA synthesis activity. Treatment with Picroside II suppressed the migratory and invasive abilities of CRC cells, accompanied by upregulation of E-cadherin and downregulation of N-cadherin, Vimentin, and ZEB2. Furthermore, Picroside II exposure led to a decrease in the expression of Notch1, Cleaved Notch1, RBP, and HES1 proteins in a concentration-dependent manner. Picroside II suppresses CRC cell progression in vitro by inhibiting the Notch1 signaling pathway, providing a preliminary molecular basis for further in vivo investigation.
PMID:42418248 | DOI:10.1002/jbt.71018
