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 (TCM) and to explore the computational molecular basis by which the liver-kidney meridian combination may support 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 collected. Data mining, network construction, network pharmacology, molecular docking, Kaplan-Meier survival analysis, and TCGA data analysis were performed to explore meridian distribution, core compounds, targets, prognostic significance, and stage-specific expression of hub genes. RESULTS The top five meridians of 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 cluster (43%), with corresponding herbs targeting the liver-kidney meridian combination. The top five key compounds were β-sitosterol, quercetin, linoleic acid, palmitic acid, and vanillic acid. Twenty-one core targets were identified, with AKT1, MYC, TP53, EGF, and MMP9 as hubs. KEGG enrichment showed involvement in PI3K-Akt pathway, platinum resistance, etc. β-sitosterol had strong binding affinity with core targets (strongest with AKT1, -33.36 kcal/mol). Survival analysis showed MYC and EGF high expression correlated with poorer pan-cancer and target tumor survival, while AKT1, TP53, and MMP9 had tumor-specific prognostic trends. Stage-specific analysis revealed core hub genes (especially MYC, AKT1) maintained stable expression across tumor stages, with no linear correlation with progression. CONCLUSION This study suggests that ovarian, cervical, and bladder cancers share a liver-kidney meridian-associated antitumor module. Liver-kidney-associated compounds, particularly β-sitosterol and quercetin, converged on PI3K-Akt and drug-resistance-related pathways through hub targets including AKT1, MYC, TP53, EGF, and MMP9. Docking supported β-sitosterol-AKT1 as a structurally plausible compound-target interaction, whereas survival analyses identified MYC and EGF as the most clinically relevant prognostic nodes. Stage-specific expression further indicated that these hub genes are not simply stage-dependent markers. Together, these findings provide a hypothesis-generating, systems-level molecular explanation for liver-kidney-based“same treatment for different diseases”in lower-jiao gynecologic and urinary tumors.