Deciphering liver-kidney meridian tropism and shared molecular modules of antitumor herbal medicines in ovarian, cervical, and bladder cancers

Objective To characterize meridian tropism patterns of antitumor traditional Chinese medicines (TCMs) and to provide a computational framework by which the liver-kidney meridian combination may inform the TCM principle of “same treatment for different diseases” in ovarian, cervical, and bladder cancers. Methods A total of 354 antitumor TCMs and 5,471 constituents were systematically curated from publicly available databases. Data mining, weighted network analysis, network pharmacology, molecular docking, Kaplan-Meier survival analysis, and TCGA-based expression profiling were integrated to examine meridian distribution, core bioactive compounds, hub targets, prognostic relevance, and stage-specific expression patterns. Results The top five meridians among antitumor TCMs were liver (21.20%), lung (16.40%), spleen (13.40%), stomach (13.20%), and kidney (10.40%). Ovarian, cervical, and bladder cancers formed the largest tumor–herb cluster (43%), predominantly associated with herbs targeting the liver-kidney meridian combination. Five core compounds—β-sitosterol, quercetin, linoleic acid, palmitic acid, and caffeic acid—were identified through weighted network topology analysis. Twenty-one intersecting targets were mapped, among which AKT1, MYC, TP53, EGF, and MMP9 emerged as hub genes. KEGG enrichment revealed predominant involvement of the PI3K-Akt signaling pathway, platinum drug resistance, and related therapeutic resistance pathways. Molecular docking demonstrated that β-sitosterol exhibited the strongest binding affinity with AKT1 (−9.34 kcal/mol) among the five hubs. Pan-cancer survival analysis showed that high MYC and EGF expression was significantly associated with poorer overall survival, whereas AKT1, TP53, and MMP9 displayed tumor-specific prognostic trends without universal significance. Stage-specific expression analysis revealed that the core hub genes—particularly MYC and AKT1—maintained relatively stable expression across tumor stages, with no statistically significant linear correlation with disease progression. Conclusion This study suggests that ovarian, cervical, and bladder cancers share a liver-kidney meridian-associated antitumor molecular pattern. Liver-kidney-associated compounds, particularly β-sitosterol and quercetin, were computationally linked to PI3K-Akt and drug-resistance pathways through hub targets including AKT1, MYC, TP53, EGF, and MMP9. Molecular docking supported β-sitosterol–AKT1 as a structurally plausible interaction, while survival analyses identified MYC and EGF as the most clinically relevant prognostic nodes. Stage-specific expression data further indicated that these hub genes function independently of tumor stage progression. Collectively, these findings provide a hypothesis-generating, systems-level computational framework for liver-kidney-based “same treatment for different diseases” in lower-jiao gynecologic and urinary tumors, although the specificity of the liver-kidney module relative to other meridian combinations awaits formal comparative validation.