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Background <p>Microplastics, particularly polystyrene (PS-MPs), are pervasive environmental pollutants linked to biological disruptions, including interference with anticancer pathways and immune regulation. Melatonin receptors (MT1, MT2) and complement regulators (Factor H, Factor I) are crucial in maintaining immune balance and cancer suppression. This study explores PS-MPs’ molecular interactions with these proteins via docking studies and evaluates their effects on colon (HCT-116) and breast (MCF-7) cancer cell lines, aiming to elucidate the health risks of microplastic exposure and potential physiological disruptions.</p> Material and methods <p>Molecular docking analyzed PS-MPs’ interactions with melatonin receptors (MT1, MT2) and complement regulators (Factor H, Factor I) using AutoDockTools. PS-MPs’ chemical structures were processed via PubChem and BABEL. HCT-116 and MCF-7 cells were cultured in DMEM, exposed to varying PS-MPs concentrations, incubated for 48 h, and analyzed microscopically.</p> Results <p>Molecular docking revealed PS-MPs as a competitive inhibitor of MT1 (−9.04 kcal/mol, Ki = 236.32 nM) and MT2 (−12.01 kcal/mol, Ki = 1.59 nM), disrupting anticancer pathways via hydrophobic interactions with key residues. PS-MPs showed moderate binding affinity to Factor H (−8.25 kcal/mol, Ki = 890.07 nM) and strong affinity to Factor I (−12.01 kcal/mol, Ki = 1.59 nM), potentially impairing immune regulation. In vitro, PS-MPs-treated HCT-116 cells displayed cytotoxic effects, including reduced density, apoptosis, and necrosis. Conversely, PS-MPs-treated MCF-7 cells showed improved adhesion, rounded morphology, and tighter clustering, suggesting enhanced substrate interaction and proliferation.</p> Conclusion <p>PS-MPs disrupt cancer suppression pathways, impairing adhesion, apoptosis, and immune regulation. These findings stress the need for regulatory measures and therapeutic strategies to counteract the health risks posed by microplastic exposure.</p> Graphical Abstract <p>PS-MPs interactions with melatonin receptors MT1, MT2, and complement proteins (Factors H, I), influencing cancer cell behavior. PS-MPs disrupt regulatory pathways in HCT-116 and MCF-7 cells, enhancing proliferation and immune evasion. Arrows depict molecular interactions leading to altered cell growth dynamics, highlighting the health risks of microplastic exposure.</p> <p></p>

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Polystyrene Microplastics Disrupt Anticancer Proteins: An In Silico and In Vitro Study

  • 期刊论文

  • 发表日期：

    2026年1月20日

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  • Ibrahim Sultan AL-Hazmi,
  • Ahmed S. Al-Shami,
  • Mohamed Gamil Mehanna,
  • Mudasir Habib Changal,
  • Ehab M. M. Ali,
  • Abdulaziz A. Kalantan,
  • Fahad A. Al Abassi,
  • Turky Omar Asar,
  • Mohd Najim,
  • Vikas Kumar,
  • Omar A. Al-Bar,
  • Firoz Anwar

摘要

Background

Microplastics, particularly polystyrene (PS-MPs), are pervasive environmental pollutants linked to biological disruptions, including interference with anticancer pathways and immune regulation. Melatonin receptors (MT1, MT2) and complement regulators (Factor H, Factor I) are crucial in maintaining immune balance and cancer suppression. This study explores PS-MPs’ molecular interactions with these proteins via docking studies and evaluates their effects on colon (HCT-116) and breast (MCF-7) cancer cell lines, aiming to elucidate the health risks of microplastic exposure and potential physiological disruptions.

Material and methods

Molecular docking analyzed PS-MPs’ interactions with melatonin receptors (MT1, MT2) and complement regulators (Factor H, Factor I) using AutoDockTools. PS-MPs’ chemical structures were processed via PubChem and BABEL. HCT-116 and MCF-7 cells were cultured in DMEM, exposed to varying PS-MPs concentrations, incubated for 48 h, and analyzed microscopically.

Results

Molecular docking revealed PS-MPs as a competitive inhibitor of MT1 (−9.04 kcal/mol, Ki = 236.32 nM) and MT2 (−12.01 kcal/mol, Ki = 1.59 nM), disrupting anticancer pathways via hydrophobic interactions with key residues. PS-MPs showed moderate binding affinity to Factor H (−8.25 kcal/mol, Ki = 890.07 nM) and strong affinity to Factor I (−12.01 kcal/mol, Ki = 1.59 nM), potentially impairing immune regulation. In vitro, PS-MPs-treated HCT-116 cells displayed cytotoxic effects, including reduced density, apoptosis, and necrosis. Conversely, PS-MPs-treated MCF-7 cells showed improved adhesion, rounded morphology, and tighter clustering, suggesting enhanced substrate interaction and proliferation.

Conclusion

PS-MPs disrupt cancer suppression pathways, impairing adhesion, apoptosis, and immune regulation. These findings stress the need for regulatory measures and therapeutic strategies to counteract the health risks posed by microplastic exposure.

Graphical Abstract

PS-MPs interactions with melatonin receptors MT1, MT2, and complement proteins (Factors H, I), influencing cancer cell behavior. PS-MPs disrupt regulatory pathways in HCT-116 and MCF-7 cells, enhancing proliferation and immune evasion. Arrows depict molecular interactions leading to altered cell growth dynamics, highlighting the health risks of microplastic exposure.