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Serum Withdrawal-Induced Apoptosis in Thyroid Cells Is Caused by Loss of Fibronectin-Integrin Interaction¹

Centro di Endocrinologia ed Oncologia Sperimentale, Consiglio Nationale delle Ricerche (G.R.); Dipartimento di Biologia e Patologia Cellulare e Molecolare (M.V., T.D., F.M., G.R.); and Dipartimento di Endocrinologia ed Oncologia Molecolare e Clinica (G.F., L.A.M.), Università Federico II, Naples 80131, Italy; and Dipartimento di Medicina Sperimentale e Clinica, Università di Catanzaro (M.B.), Catanzaro 88100, Italy

Address all correspondence and requests for reprints to: Dr. Mario Vitale, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Via S. Pansini 5, Naples 80131, Italy. E-mail: mavitale{at}unina.it

In some cell types, including a fetal thyroid cell line, denial of adhesion to extracellular matrix induces a type of apoptosis called anoikis. Serum withdrawal in dog and transformed rat thyroid cells also induces programmed cell death. Because serum can stimulate cells to produce some components of the extracellular matrix, it was of interest to determine the role of the matrix in the apoptosis induced by serum withdrawal in normal human thyroid cells in primary culture. The present report demonstrates that thyroid cells selectively produce and deposit insoluble fibronectin (FN) only when stimulated by serum. Adhesion in the presence of serum is dependent upon integrin-FN interaction. Serum withdrawal determines a degradation of the insoluble FN deposited and a detachment of the cells from the plates. In these conditions, cells undergo anoikis, demonstrated by DNA fragmentation and annexin V staining. Apoptosis was prevented by exogenous FN immobilized onto the plates. These results indicate that serum withdrawal induces apoptosis in human thyroid cells, determining FN degradation and loss of cell-matrix adhesion.

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