ArticleFrontiers in pharmacology2026
Integrated multi-omics analysis suggests the involvement of PI3K-Akt/p21 signaling in the anti-colorectal cancer effects of
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, underscoring the need for more effective and well-tolerated therapeutic strategies. Methods: Network pharmacology, molecular docking, and label-free proteomics were combined with cell-based assays. Functional relevance of AKT signaling was evaluated using siRNA knockdown, MK2206, and SC79. Results: Fifty-three putative bioactive compounds and 154 CRC-related targets were identified, with AKT1, EGFR, and SRC emerging as candidate hub proteins. EEDJF significantly inhibited proliferation in HCT116 and SW480 colorectal cancer cells, induced apoptosis, and promoted G1/S cell cycle arrest. In contrast, EEDJF showed minimal cytotoxicity toward HaCaT epithelial cells under the tested conditions. Proteomic and enrichment analyses consistently highlighted the PI3K-Akt-related signaling among the most significantly associated pathways. Modulation of AKT activity altered the cellular response to EEDJF, supporting the involvement of this pathway. Conclusion: EEDJF exerts anti-colorectal cancer effects
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