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Retroelements in thyroid cancer: epigenetic plasticity, dedifferentiation, and therapeutic opportunities

Nathália Da Roz D'Alessandre1, Bruna Sousa Pessoa2, Gabriela Der Agopian Guardia1

  • 1Centro de Oncologia Molecular, Hospital Sírio-Libanês, São Paulo, 01308-060, SP, Brazil.

Reviews in Endocrine & Metabolic Disorders
|November 26, 2025
PubMed

Insights

Thyroid tumors evolve through genetic changes and reactivated mobile genetic elements, like retroelements. Suppressing these elements offers a potential new therapeutic strategy for aggressive thyroid cancer.

Area of Science:

  • Oncology
  • Genetics
  • Epigenetics

Background:

  • Thyroid tumors exhibit significant phenotypic plasticity, progressing from differentiated to aggressive anaplastic subtypes.
  • Classical genetic drivers (BRAF, TP53, RAS) explain some oncogenic transitions but not the full extent of transcriptional deregulation and therapeutic resistance in advanced disease.
  • Mobile genetic elements (MGEs), including LINE-1 retrotransposons and human endogenous retroviruses, comprise nearly half the genome and are normally silenced.

Purpose of the Study:

  • To explore the role of MGEs in thyroid tumor evolution and therapeutic resistance.
  • To connect genetic alterations with MGE reactivation and phenotypic dedifferentiation.
  • To identify MGEs as potential biomarkers and therapeutic targets in thyroid cancer.

Main Methods:

  • Review of existing literature integrating cancer epigenetics and mobilome biology.
  • Analysis of the functional connection between genetic alterations (TERT promoter mutations, TP53 dysfunction) and MGE reactivation.
  • Examination of emerging data on reverse transcriptase inhibitors' effects on retroelement activity.

Main Results:

  • Aberrant MGE reactivation, driven by epigenetic erosion and genetic alterations, contributes to non-canonical transcripts, regulatory rewiring, and insertional mutagenesis.
  • TP53 dysfunction and TERT promoter mutations are linked to LINE-1 and endogenous retroviral element derepression, respectively.
  • Reverse transcriptase inhibitors show potential in suppressing MGE activity, inducing transcriptional reprogramming, and restoring radioiodine uptake in refractory thyroid tumors.

Conclusions:

  • Thyroid tumor evolution is influenced by both genetic alterations and retroelement-mediated disruption of genome regulation.
  • MGEs represent potential biomarkers for aggressive thyroid tumor transformation.
  • Targeting MGEs offers a novel therapeutic vulnerability in translational oncology for thyroid cancer.
Keywords:
Anaplastic thyroid carcinomaHERVHuman endogenous retrovirusesLINE-1Radioiodine-refractory cancerThyroid cancer

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