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Peer-reviewedCC BYFrontiers in oncology

Exploring the mechanisms of baicalein in lung adenocarcinoma: an integrative preliminary study with focused experimental assessment in A549 cells.

  • Jiaqian Yuan1
  • Jiayan Zhong2
  • Ruilin Chen2
  • Jia Mao3
  • Zhen Wang2
  1. 1The First School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
  2. 2Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
  3. 3Department of Respiratory and Critical Care Medicine, Ningbo TCM Hospital Affiliated to Zhejiang Chinese Medical University, Ningbo, China.
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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 Scutellaria baicalensis Georgi, shows antitumor potential, yet integrative and immune-related evaluations of BA in LUAD remain limited.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 in vitro, with IC₅₀ values of 54.93 μM at 24 h and 22.83 μM at 48 h. Among the prioritized candidates, AKT1 and BCL2 were selected for focused experimental assessment in A549 cells. BA treatment reduced AKT1 phosphorylation and BCL2 protein expression in A549 cells, whereas total AKT1 remained largely unchanged. HIF1A expression showed broad associations with computationally estimated immune-cell fractions and poorer overall survival.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 in vitro, and the observed changes in AKT1 phosphorylation and BCL2 protein expression provide focused experimental support for selected components of the candidate network; further in vitro and in vivo studies are required to validate biological relevance and translational potential.

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Cite

BibTeXRIS
BibTeX
@article{yuan2026exploring,
  title = {{Exploring the mechanisms of baicalein in lung adenocarcinoma: an integrative preliminary study with focused experimental assessment in A549 cells.}},
  author = {Jiaqian Yuan and Jiayan Zhong and Ruilin Chen and Jia Mao and Zhen Wang},
  journal = {Frontiers in oncology},
  year = {2026},
  month = oct,
  doi = {10.3389/fonc.2026.1912108},
  url = {https://europepmc.org/article/MED/42903066},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Exploring the mechanisms of baicalein in lung adenocarcinoma: an integrative preliminary study with focused experimental assessment in A549 cells.
AU  - Jiaqian Yuan
AU  - Jiayan Zhong
AU  - Ruilin Chen
AU  - Jia Mao
AU  - Zhen Wang
PY  - 2026
DA  - 2026/10/06
JO  - Frontiers in oncology
DO  - 10.3389/fonc.2026.1912108
UR  - https://europepmc.org/article/MED/42903066
AB  - 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 Scutellaria baicalensis Georgi, shows antitumor potential, yet integrative and immune-related evaluations of BA in LUAD remain limited.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 in vitro, with IC₅₀ values of 54.93 μM at 24 h and 22.83 μM at 48 h. Among the prioritized candidates, AKT1 and BCL2 were selected for focused experimental assessment in A549 cells. BA treatment reduced AKT1 phosphorylation and BCL2 protein expression in A549 cells, whereas total AKT1 remained largely unchanged. HIF1A expression showed broad associations with computationally estimated immune-cell fractions and poorer overall survival.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 in vitro, and the observed changes in AKT1 phosphorylation and BCL2 protein expression provide focused experimental support for selected components of the candidate network; further in vitro and in vivo studies are required to validate biological relevance and translational potential.
SN  - 2234-943X
ER  -