Molecular mechanisms of lung cancer induced by the insecticide lambda-cyhalothrin.

Yongshun DUAN; Zifei WANG; Mengxuan WU; Shuo WANG; Xin GUO; Zhihua NI

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Molecular mechanisms of lung cancer induced by the insecticide lambda-cyhalothrin.

Author: Yongshun DUAN ¹ ; Zifei WANG ¹ ; Mengxuan WU ¹ ; Shuo WANG ¹ ; Xin GUO ¹ ; Zhihua NI ¹
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1. College of Life Sciences, Hebei University, Baoding 071002, Hebei, China.
Publication Type:Journal Article
Keywords: lambda-cyhalothrin; lung cancer; molecular docking; molecular mechanism; network toxicology
MeSH: Lung Neoplasms/metabolism*; Pyrethrins/toxicity*; Humans; Insecticides/toxicity*; Nitriles/toxicity*; Molecular Docking Simulation
From: Chinese Journal of Biotechnology 2025;41(10):3801-3816
CountryChina
Language:Chinese
Abstract: The inappropriate utilisation of the agricultural insecticide lambda-cyhalothrin (LCT) has the potential to result in residues that compromise food safety and human health. Respiratory exposure represents a major route of LCT contact in humans. Nevertheless, its deleterious effects on the respiratory system remain inadequately characterized. It is imperative to elucidate the potential relationship and mechanisms by which lung cancer, a significant malignant neoplasm of the respiratory system, is associated with exposure to LCT. The objective of this study is to utilise bioinformatics methodologies to screen and analyse the key target molecules affected by LCT in the occurrence of lung cancer, and their mechanisms of action. Specifically, network toxicology methods were employed to identify core targets of LCT-induced lung cancer. Subsequently, functional annotation to delineate associated cellular pathways, and finally, molecular docking to simulate binding modes between LCT and shared core targets. Core target screening identified 50 targets for large cell lung cancer, 54 for small cell lung cancer, 29 for lung squamous cell carcinoma, and 28 for lung adenocarcinoma, with EGFR, HSP90AA1, JUN, CCL2, MYC, CXCL8, and HSPA4 shared in all subtypes. Functional annotation revealed that LCT-triggered oncogenic pathways predominantly involved ubiquitination, chemotaxis, and tumor immune signaling. Molecular docking demonstrated spontaneous binding of LCT to core targets mediated by hydrogen bonds and π-cation interactions. These results establish a theoretical framework for evaluating LCT-associated risks of lung cancer and respiratory system damage.