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Mutual regulation of TGF-β1, TβRII and ErbB receptors expression in human thyroid carcinomas

Gabriella Mincione1, Chiara Tarantelli2, Giovina Vianale1

  • 1Department of Experimental and Clinical Sciences, University 'G. d'Annunzio of Chieti-Pescara, Chieti, Italy; Center of Excellence on Aging, Ce.S.I., 'G. d׳Annunzio' University Foundation, Chieti, Italy.

Experimental Cell Research
|June 29, 2014
PubMed

Insights

Epidermal Growth Factor (EGF) and Transforming Growth Factor-beta 1 (TGF-β1) signaling pathways influence thyroid cancer progression. Their interaction, particularly in follicular thyroid carcinoma, suggests a complex role in tumor cell migration and aggressive behavior.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • The precise roles of Epidermal Growth Factor (EGF) and Transforming Growth Factor-beta 1 (TGF-β1) in thyroid cancer remain unclear.
  • Previous studies suggest TGF-β1 can inhibit thyroid cancer cell growth and migration.

Purpose of the Study:

  • To investigate the combined effects of EGF and TGF-β1 on thyroid cancer cell lines.
  • To analyze the expression of TGF-β1, TGF-beta Receptor II (TβRII), and Epidermal Growth Factor Receptor (EGFR) in benign and malignant thyroid tumors.
  • To explore the relationship between these factors and tumor aggressiveness, including E-cadherin expression.

Main Methods:

  • Utilized follicular (FTC-133) and papillary (B-CPAP) thyroid carcinoma cell lines for in vitro experiments.
  • Administered co-treatments of TGF-β1 and EGF to assess cellular proliferation and migration.
  • Employed MAPK pathway analysis to understand the mechanism of action.
  • Performed quantitative analysis of TGF-β1, TβRII, and EGFR mRNA expression in thyroid tumor tissues (follicular adenoma, papillary carcinoma, follicular carcinoma).
  • Assessed E-cadherin expression in tumor samples.

Main Results:

  • TGF-β1 inhibited proliferation and migration in both cell lines.
  • Co-treatment with EGF and TGF-β1 inhibited proliferation but differentially affected migration: inhibition in B-CPAP cells and promotion in FTC-133 cells via a MAPK-dependent pathway.
  • EGFR mRNA overexpression correlated with aggressive tumor behavior across follicular adenoma, papillary carcinoma, and follicular carcinoma.
  • TGF-β1 and TβRII mRNA were moderately overexpressed in papillary carcinoma but highly overexpressed in follicular carcinoma.
  • Follicular carcinomas showed a loss of E-cadherin expression, unlike papillary carcinomas.

Conclusions:

  • A cross-talk between EGF and TGF-β1 signaling pathways is implicated in the phenotype of follicular thyroid carcinomas.
  • Overexpression of TGF-β1/TβRII and EGFR, coupled with E-cadherin loss, characterizes aggressive follicular thyroid carcinomas.
  • The MAPK-dependent increase in migration following EGF/TGF-β1 treatment in FTC-133 cells supports their role in follicular thyroid carcinoma progression.
Keywords:
EGFErbB receptorsHuman thyroid carcinomaTGF-β1TβRII

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