ArticleFrontiers in oncology2026
Exploring the mechanisms of baicalein in lung adenocarcinoma: an integrative preliminary study with focused experimental assessment in A549 cells.
Article in Frontiers in oncology, 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: Lung adenocarcinoma (LUAD) continues to present therapeutic challenges because of pathway redundancy and treatment resistance, underscoring the need for multi-target and systems-level strategies. Baicalein (BA), a flavonoid metabolite from Methods: We integrated network analyses with TCGA-LUAD transcriptomics, weighted gene co-expression network analysis (WGCNA), network topology, GO/KEGG enrichment, bulk RNA-seq-based immune-infiltration estimation (CIBERSORT), molecular docking, and clinical association analysis (GEPIA2/HPA). Cell viability was assessed in A549 cells using the CCK-8 assay, and AKT1 phosphorylation and BCL2 protein expression were further examined experimentally by western blot analysis. Results: A total of 117 candidate BA-LUAD overlapping targets were identified, and six candidate hub genes (EGFR, AKT1, TP53, BCL2, HIF1A, and ESR1) were prioritized. Enrichment analyses suggested that the candidate network was associated with oncogenic signaling and stress-response programs, particularly PI3K-AKT/MAPK signaling, ROS-related processes, apoptosis, and p53 signaling. CCK-8 assays showed that BA reduced A549 cell viability Conclusion: These findings prioritize a BA-associated candidate network in LUAD involving kinase signaling, apoptosis-related regulation, oxidative-stress responses, and immune-microenvironment associations. The CCK-8 results support an inhibitory effect of BA on A549 cell viability
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