Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study
By
Xiao-Jue Huang
Liu-Hui Mo
Ke-Jun Wu
Rong-Quan He
Hui Li
Gang Chen
Li-Min Liu
May 12, 2026
Clinical Scorecard: Nitidine chloride inhibits polo-like kinase 1 through MYCN-related transcriptional mechanisms in colorectal cancer: insights from multi-omics and spatial transcriptomics analysis
At a Glance
Category Detail
Condition Colorectal Cancer (CRC) Key Mechanisms Inhibition of Polo-like kinase 1 (PLK1) through MYCN-related transcriptional mechanisms Target Population Patients with colorectal cancer Care Setting Oncology research and clinical settings
Key Highlights
Nitidine chloride (NC) significantly reduces PLK1 expression in CRC. PLK1 is overexpressed in CRC and associated with poor prognosis. MYCN is positively correlated with PLK1 expression in CRC. NC treatment downregulates both PLK1 and MYCN. Multi-omics analysis reveals PLK1 as a key target of NC. Guideline-Based Recommendations
Diagnosis
Utilize RNA sequencing and multi-omics approaches for CRC diagnosis. Management
Consider nitidine chloride as a potential therapeutic agent targeting PLK1 in CRC. Monitoring & Follow-up
Monitor PLK1 and MYCN expression levels in CRC patients undergoing treatment. Risks
Be aware of the potential for toxicity with standard chemotherapeutics like 5-FU. Patient & Prescribing Data
Patients diagnosed with colorectal cancer, particularly those with PLK1 overexpression.
Nitidine chloride shows promise in reducing PLK1 levels and may enhance therapeutic outcomes.
Clinical Best Practices
Integrate multi-omics data for personalized treatment strategies in CRC. Evaluate the expression of PLK1 and MYCN as biomarkers for treatment response. Related Resources & Content
