Mutual regulation of TGF-beta 1, T beta RII and ErbB receptors expression in human thyroid carcinomas

作者:Mincione Gabriella*; Tarantelli Chiara; Vi****e Giovina; Di Marcantonio Maria Carmela; Cotellese Roberto; Francomano Franco; Di Nicola Marta; Costantini Erica; Cichella Annadomenica; Muraro Raffaella
来源:Experimental Cell Research, 2014, 327(1): 24-36.
DOI:10.1016/j.yexcr.2014.06.012

摘要

The role of EGF and TGF-beta 1 in thyroid cancer is still not clearly defined. TGF-beta 1 inhibited the cellular growth and migration of follicular (FTC-133) and papillary (B-CPAP) thyroid carcinoma cell lines. Co-treatments of TGF-beta 1 and EGF inhibited proliferation in both cell lines, but displayed opposite effect on their migratory capability, leading to inhibition in B-CPAP and promotion in FTC-133 cells, by a MAPK-dependent mechanism. TGF-beta 1, T beta RII and EGFR expressions were evaluated in benign and malignant thyroid tumors. Both positivity (51.7% and 60.0% and 80.0% in FA and FTC and FTC) and overexpression (60.0%, 77.7% and 75.0% in FA, FTC and FTC) of EGFR mRNA correlates with the aggressive tumor behavior. The moderate overexpression of TGF-beta 1 and T beta RII mRNA in FTC tissues (615% and 62.5%, respectively), counteracted their high overexpression in FTC tissues (100% and 100%, respectively), while EGFR overexpression was similar in both carcinomas. Papillary carcinomas were positive to E-cadherin expression, while the follicular carcinomas lose E-cadherin staining. Our findings of TGF-beta 1/T beta RII and EGFR overexpressions together with a loss of E-cadherin observed in human follicular thyroid carcinomas, and of increased migration ability MAPK-dependent after EGF/TGF-beta 1 treatments in the follicular thyroid carcinoma cell line, reinforced the hypothesis of a cross-talk between EGF and TGF-beta 1 systems in follicular thyroid carcinomas phenotype.

  • 出版日期2014-9-10