Anethole suppresses proliferation and migration of lung adenocarcinoma cells and modulates ESRβ/SRC/EGFR-related signaling
- 1Department of Thoracic Surgery, First Affiliated Hospital of Jinzhou Medical University
Abstract
Despite advances in lung adenocarcinoma (LUAD) treatment, therapeutic efficacy remains limited and recurrence remains common, highlighting the need for additional therapeutic strategies. This study integrated network pharmacology, molecular docking, and in vitro assays to explore the potential anti-LUAD activity of anethole and its associated signaling changes. Potential targets of anethole were predicted using PharmMapper and intersected with LUAD-related targets obtained from GeneCards, yielding 44 overlapping targets. A protein–protein interaction network and GO/KEGG enrichment analyses suggested that estrogen receptor-related and SRC-associated signaling may be relevant to the response to anethole. Molecular docking provided computational evidence of possible interactions between anethole and selected candidate proteins, including ESRβ and SRC. In vitro assays showed that anethole reduced the viability and EdU incorporation of H1975 and PC-9 cells, impaired the survival or growth of pre-formed colonies, induced G0/G1-phase cell-cycle arrest, and reduced wound closure and transwell migration under the tested conditions. Western blot analysis showed decreased ESRβ expression and reduced phosphorylation of SRC and EGFR, accompanied by reduced activation of PI3K/AKT and MEK/ERK signaling. These findings suggest that anethole suppresses malignant phenotypes of LUAD cells and may modulate ESRβ/SRC/EGFR-related signaling.
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BibTeX
@article{sun2026anethole,
title = {{Anethole suppresses proliferation and migration of lung adenocarcinoma cells and modulates ESRβ/SRC/EGFR-related signaling}},
author = {Yinghuan Sun and Jiacheng Zhu and Pengcheng Qiu and Zhenjie Sun and Kemu Zhang and Hongli Zhou and Bo Huang},
journal = {Discover Oncology},
year = {2026},
month = jul,
doi = {10.1007/s12672-026-05607-8},
url = {https://doi.org/10.1007/s12672-026-05607-8},
note = {CC BY},
}
RIS
TY - JOUR
TI - Anethole suppresses proliferation and migration of lung adenocarcinoma cells and modulates ESRβ/SRC/EGFR-related signaling
AU - Yinghuan Sun
AU - Jiacheng Zhu
AU - Pengcheng Qiu
AU - Zhenjie Sun
AU - Kemu Zhang
AU - Hongli Zhou
AU - Bo Huang
PY - 2026
DA - 2026/07/01
JO - Discover Oncology
DO - 10.1007/s12672-026-05607-8
UR - https://doi.org/10.1007/s12672-026-05607-8
AB - Despite advances in lung adenocarcinoma (LUAD) treatment, therapeutic efficacy remains limited and recurrence remains common, highlighting the need for additional therapeutic strategies. This study integrated network pharmacology, molecular docking, and in vitro assays to explore the potential anti-LUAD activity of anethole and its associated signaling changes. Potential targets of anethole were predicted using PharmMapper and intersected with LUAD-related targets obtained from GeneCards, yielding 44 overlapping targets. A protein–protein interaction network and GO/KEGG enrichment analyses suggested that estrogen receptor-related and SRC-associated signaling may be relevant to the response to anethole. Molecular docking provided computational evidence of possible interactions between anethole and selected candidate proteins, including ESRβ and SRC. In vitro assays showed that anethole reduced the viability and EdU incorporation of H1975 and PC-9 cells, impaired the survival or growth of pre-formed colonies, induced G0/G1-phase cell-cycle arrest, and reduced wound closure and transwell migration under the tested conditions. Western blot analysis showed decreased ESRβ expression and reduced phosphorylation of SRC and EGFR, accompanied by reduced activation of PI3K/AKT and MEK/ERK signaling. These findings suggest that anethole suppresses malignant phenotypes of LUAD cells and may modulate ESRβ/SRC/EGFR-related signaling.
SN - 2730-6011
ER -