Translational study demonstrates nitidine chloride suppresses colorectal cancer progression by downregulating KIF11, indicating a potential targeted therapeutic strategy.
Key Points
To assess the clinical relevance of KIF11 overexpression in colorectal cancer and investigate whether nitidine chloride suppresses tumor progression via the KIF11 pathway.
Analyzed KIF11 expression using public datasets, single-cell RNA sequencing, spatial transcriptomics, and immunohistochemistry on 416 clinical colorectal cancer specimens.
Investigated nitidine chloride binding using molecular docking and characterized the functional effects of KIF11 silencing via CRISPR knockout and lentiviral knockdown.
Meta-analysis confirmed KIF11 mRNA overexpression (SMD = 1.33; AUC = 0.87), while protein analysis in 416 clinical specimens showed marked elevation (AUC = 0.99) correlating with larger tumor size and deeper invasion.
Nitidine chloride exhibited strong docking affinity for KIF11 (-9.0 kcal/mol), and KIF11 depletion halted cell-cycle progression at the G2/M phase via the RAD21–KIF11 regulatory axis.