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The PARP inhibitor PJ34 modifies proliferation, NIS expression and epigenetic marks in thyroid cancer cell lines

Elisa Lavarone1, Cinzia Puppin, Nadia Passon

  • 1Dipartimento di Scienze Mediche e Biologiche, Università di Udine, Udine, Italy.

Molecular and Cellular Endocrinology
|September 18, 2012
PubMed

Insights

PARP inhibition with PJ34 significantly boosts sodium iodide symporter (NIS) expression and radio-iodine uptake in thyroid cancer cells. This suggests PARP inhibitors could be a novel therapeutic strategy for thyroid cancer treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Endocrinology

Background:

  • Poly(ADP-ribose) polymerase-1 (PARP-1) is implicated in repressing sodium iodide symporter (NIS) expression.
  • Thyroid cancer treatment can be advanced by enhancing NIS expression and radio-iodine uptake.

Purpose of the Study:

  • To investigate the effect of the PARP inhibitor PJ34 on NIS expression and related properties in thyroid cancer cell lines.
  • To explore the underlying transcriptional regulatory mechanisms, including epigenetic modifications.

Main Methods:

  • Treatment of thyroid cancer cell lines (TPC1, BCPAP, FRO, WRO) with the PARP inhibitor PJ34.
  • Analysis of NIS mRNA levels, radio-iodine uptake, and NIS promoter activity.
  • Investigation of histone modifications (H3K9K14ac, H3K4me3, H3K27me3) at the NIS promoter.

Main Results:

  • PJ34 treatment strongly increased NIS mRNA levels in all tested cell lines.
  • Significant enhancement of radio-iodine uptake was observed in BCPAP and TPC1 cells.
  • PJ34 increased NIS promoter activity and altered histone marks, including an unexpected rise in H3K27me3.

Conclusions:

  • PARP inhibition by PJ34 effectively increases NIS gene expression in thyroid cancer cells.
  • The mechanism involves unique modulation of transcriptional regulation and epigenetic modifications.
  • PARP inhibitors show promise as a potential therapeutic approach for thyroid cancer.

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