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Nitenpyram promotes breast cancer progression via PARP1: Integration of multi-omics analyses with experimental
Dongliang Yin1, Haoyu Qin2, Menglan Yan3
1Affiliated Rehabilitation Hospital of Nanchang University, Nanchang, Jiangxi, China.
Abstract:
Nitenpyram (NIT) is an insecticide used primarily for flea control in pets, especially cats and dogs. Some studies suggest that NIT is associated with cancer development, but the mechanisms involved are unclear. In this study, we integrated multi-platform bioinformatics analysis, protein-protein interaction (PPI) network construction, gene enrichment analysis and molecular docking to explore the carcinogenic mechanism of NIT in depth. We first targeted the oncogenic targets under NIT exposure, and then mapped the cross-cancer expression profiles based on 26 core genes, and quantitatively analyzed the impact weights of these genes on the prognosis of multiple malignant tumors with the help of machine learning models. Molecular docking suggested potential interactions between NIT and six proteins (KRAS, PARP1, KIT, ITGB1, EGFR, and CXCR4), with predicted binding energies below -6 kcal/mol. Single-cell transcriptomic data indicated that these genes are mainly expressed in T cells, B cells, and other immune cell subsets. Disruption of these molecules by NIT may result in reduced genetic stability, immune imbalance and disruption of cellular homeostasis, providing favorable conditions for cancer development. Finally, through integrating protein quantification analysis and cell colony formation assays, we confirmed that exposure to NIT promotes the proliferation of breast cancer cells, concomitant with an increase in PARP1 expression. Notably, short-term exposure to high doses of NIT exerts a more pronounced effect on cell proliferation.
Insights
Nitenpyram (NIT), a common flea treatment, may promote cancer by disrupting immune cells and genetic stability. High doses of NIT significantly increase breast cancer cell proliferation, linked to PARP1 expression.
Area of Science:
- Toxicology
- Molecular Biology
- Bioinformatics
Background:
- Nitenpyram (NIT) is widely used for flea control in pets.
- Previous studies suggest a potential link between NIT exposure and cancer, but underlying mechanisms remain unclear.
Purpose of the Study:
- To investigate the carcinogenic mechanisms of Nitenpyram (NIT) using multi-platform bioinformatics and experimental approaches.
- To identify key molecular targets and pathways involved in NIT-induced carcinogenesis.
Main Methods:
- Integrated bioinformatics analysis, including protein-protein interaction (PPI) network construction and gene enrichment analysis.
- Molecular docking to predict interactions between NIT and oncogenic proteins.
- Single-cell transcriptomic analysis to determine gene expression in immune cells.
- Cellular assays (protein quantification, colony formation) to validate findings in breast cancer models.
Main Results:
- Identified 26 core genes associated with NIT exposure and mapped their cross-cancer expression profiles.
- Molecular docking revealed potential interactions of NIT with KRAS, PARP1, KIT, ITGB1, EGFR, and CXCR4.
- These genes are predominantly expressed in immune cells (T cells, B cells).
- NIT exposure promoted breast cancer cell proliferation and increased PARP1 expression, with higher doses showing a more pronounced effect.
Conclusions:
- Nitenpyram (NIT) may contribute to cancer development by compromising genetic stability and immune balance.
- NIT directly interacts with key proteins involved in cell signaling and proliferation.
- Experimental evidence confirms NIT promotes breast cancer cell proliferation, highlighting PARP1 as a potential mediator.
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