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Atrazine-induced carcinogenesis in colorectal cancer: Core gene identification, immune cell infiltration, and
Laiming Mo1, Siyang Yu1, Huijun Zhu2
1Department of Clinical Laboratory, The Seventh Affiliated Hospital of Sun Yat-Sen University, Guangming District, Shenzhen, Guangdong 518107, China.
Objective:
To explore the molecular mechanisms underlying the role of the environmental pollutant Atrazine in promoting colorectal cancer (CRC) tumorigenesis and progression.
Methods:
The toxicological properties of Atrazine were evaluated using ADMETlab 3.0 and ProTox-3.0. Potential targets were predicted through SuperPred, TargetNet, SwissTargetPrediction, and STITCH databases, then intersected with CRC-related genes from GeneCards, TTD, and OMIM to identify candidate toxicological targets. GO, KEGG, and Metascape analyses were conducted to explore biological functions and signaling pathways. Transcriptomic data from the GEO database were integrated to construct 112 machine learning models for identifying Atrazine-related core genes. Gene expression and protein localization were verified through standardized mean difference analysis and the HPA database. A logistic regression-based nomogram was established to assess the diagnostic performance of core genes. Molecular docking using CB-Dock2 was applied to evaluate binding affinity between Atrazine and target proteins, while GSEA identified pathways associated with core gene expression. Immune infiltration and single-cell expression profiles were analyzed using CIBERSORT and TISCH2 databases. Finally, SHAP analysis was performed to determine the relative contribution of each gene to the predictive model, and in vitro assays were conducted to validate the functional effects of Atrazine exposure on CRC cells.
Results:
Atrazine exhibited remarkable carcinogenicity and multi-system toxicity. Functional enrichment indicated significant involvement of candidate targets in oxidative stress, inflammation, apoptosis regulation, and immune evasion. Machine learning identified six core genes. Among them, MMP7, GSTP1, MIF, and ABCC1 were upregulated, while SGK1 and PTGS1 were downregulated in CRC. The nomogram model showed excellent predictive accuracy. SHAP analysis further revealed ABCC1, SGK1, and GSTP1 as key contributors, with ABCC1 exhibiting the highest SHAP value and the strongest binding affinity with Atrazine. CCK-8 and wound healing assays confirmed that Atrazine exposure enhanced CRC cell proliferation and migration, while qPCR analysis showed significant upregulation of ABCC1 expression in HCT116 and SW480 cells.
Conclusion:
Atrazine promotes CRC progression through multi-target and multi-pathway mechanisms. ABCC1 serves as the central gene linking Atrazine exposure to enhanced proliferation and migration of CRC cells.
Insights
The environmental pollutant Atrazine promotes colorectal cancer (CRC) by affecting multiple molecular targets and pathways. ABCC1 is identified as a key gene linking Atrazine exposure to increased CRC cell proliferation and migration.
Area of Science:
- Environmental Toxicology
- Cancer Biology
- Molecular Mechanisms
Background:
- Atrazine is an environmental pollutant with suspected carcinogenic properties.
- Colorectal cancer (CRC) is a significant global health concern.
- Understanding the molecular link between environmental factors and cancer is crucial for prevention and treatment.
Purpose of the Study:
- To elucidate the molecular mechanisms by which Atrazine promotes colorectal cancer (CRC) tumorigenesis and progression.
- To identify key genes and pathways involved in Atrazine-induced CRC.
Main Methods:
- In silico toxicological assessments (ADMETlab, ProTox), target prediction (SuperPred, TargetNet, SwissTargetPrediction, STITCH), and pathway analysis (GO, KEGG, Metascape).
- Machine learning models using transcriptomic data (GEO) to identify core genes, validated by gene expression and protein localization data (HPA).
- Molecular docking (CB-Dock2), nomogram construction, GSEA, immune infiltration analysis (CIBERSORT, TISCH2), SHAP analysis, and in vitro functional assays (CCK-8, wound healing, qPCR).
Main Results:
- Atrazine demonstrated significant carcinogenicity and multi-system toxicity.
- Six core genes were identified, with ABCC1, MMP7, GSTP1, and MIF upregulated, and SGK1 and PTGS1 downregulated in CRC.
- ABCC1 showed the strongest binding affinity with Atrazine and was identified as a key contributor to CRC progression, enhancing cell proliferation and migration.
- In vitro assays confirmed Atrazine's role in promoting CRC cell growth and motility, with significant ABCC1 upregulation.
Conclusions:
- Atrazine promotes CRC progression via multi-target and multi-pathway mechanisms.
- ABCC1 is a central gene mediating the effects of Atrazine on CRC cell proliferation and migration.
- These findings highlight the oncogenic role of Atrazine and identify ABCC1 as a potential therapeutic target.
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