The v-erbA oncogene selectively inhibits iodide uptake in rat thyroid cells

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F Trapasso1, M L Martelli, C Battaglia

  • 1Dipartimento di Medicina Sperimentale e Clinica, Facoltà di Medicina eChirurgia di Cantanzaro, Università degli Studi di Reggio Calabria, Italy.

Oncogene
|May 2, 1996
PubMed

Insights

The v-erbA oncogene inhibits thyroid cell growth and iodide uptake by activating transcription factor AP-1. This transcriptional activation explains v-erbA

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Oncology

Background:

  • v-erbA is an oncogenic form of the c-erbA proto-oncogene, encoding the thyroid hormone receptor.
  • Thyroid-differentiated cells (PC Cl 3) are used to study oncogene effects.

Purpose of the Study:

  • To investigate the selective effects of v-erbA oncogene expression on thyroid-differentiated cells.
  • To determine the role of transcription factor AP-1 in mediating v-erbA's effects.

Main Methods:

  • Expression of v-erbA in PC Cl 3 cells.
  • Assay of iodide uptake and thyrotropin-dependent growth.
  • Measurement of thyroid-specific marker expression (thyroglobulin, thyroperoxidase, thyrotropin receptor).
  • DNA binding assays and reporter gene transcription assays for AP-1 activity.
  • Analysis of v-erbA mutants lacking DNA binding domain activity.

Main Results:

  • v-erbA expression inhibited iodide uptake and thyrotropin-dependent growth in PC Cl 3 cells.
  • Thyroid-specific markers (thyroglobulin, thyroperoxidase, thyrotropin receptor) were unaffected by v-erbA.
  • AP-1 activity was enhanced in PC v-erbA cells.
  • v-erbA mutants lacking DNA binding domain did not affect iodide uptake or AP-1 activity.

Conclusions:

  • v-erbA selectively impacts thyroid cell function, inhibiting iodide uptake and growth.
  • Transcriptional activation mediated by AP-1 is the likely mechanism for v-erbA's selective effects on thyroid-specific gene expression.

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