Organochlorine pesticides and epigenetic alterations in thyroid tumors

Fouzieh Salimi1,2,3, Gholamreza Asadikaram2,3, Mohammad Reza Ashrafi2,3

  • 1Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences Kerman University of Medical Sciences, Kerman, Iran.

PubMed
Abstract

Insights

Organochlorine pesticides (OCPs) exposure is linked to papillary thyroid carcinoma (PTC) progression. OCPs increase TSHR methylation and decrease H3K9/H4K16 acetylation, suggesting predictive value in PTC patients.

Area of Science:

  • Environmental Epigenetics
  • Cancer Biology
  • Toxicology

Background:

  • Cancer incidence is influenced by environmental factors like pesticide exposure, which can induce epigenetic alterations.
  • Organochlorine pesticides (OCPs) are persistent environmental pollutants with potential links to various health issues, including cancer.

Purpose of the Study:

  • To investigate the impact of organochlorine pesticides (OCPs) on the promoter methylation of three tumor-suppressor genes (TSHR, ATM, P16) and four histone modifications in patients with papillary thyroid carcinoma (PTC) and benign thyroid nodules (BTN).

Main Methods:

  • OCPs were quantified using Gas Chromatography.
  • Promoter methylation of TSHR, ATM, and P16 genes was assessed via nested-methylation-specific PCR (MSP).
  • Histone modifications, including acetylation (H3K9, H4K16, H3K18) and methylation (H4K20), were detected using Western blot analysis.

Main Results:

  • Papillary thyroid carcinoma (PTC) samples showed increased TSHR promoter methylation and decreased P16 methylation compared to benign thyroid nodules (BTN).
  • Organochlorine pesticide (OCP) exposure significantly increased the odds of TSHR and P16 methylation.
  • PTC samples exhibited hypomethylation of H4K20 and hypo-acetylation of H3K9, H4K16, and H3K18, with OCPs decreasing the odds of H3K9 and H4K16 acetylation.

Conclusions:

  • Organochlorine pesticides (OCPs) may contribute to papillary thyroid carcinoma (PTC) progression through TSHR promoter hypermethylation and reduced H3K9/H4K16 acetylation.
  • Assessing TSHR promoter methylation and H3K9/H4K16 acetylation in PTC patients may offer predictive value for the disease.

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