Tenascin‐C, a 6‐armed extracellular matrix glycoprotein, is expressed in a temporally and spatially restricted pattern during tumorigenesis in association with stromal‐epithelial interactions. We have previously shown that de novo synthesis of tenascin‐C is induced by the diffusible factor EGF in tenascin‐C‐non‐producing human epidermoid carcinoma cells in stromal‐epithelial interactions. We now demonstrate that the addition of human tenascin‐C or tenascin‐C peptides to the culture medium of these cells had little effect on the induction of tenascin‐C. The physiological regulators of tenascin‐C induction through the EGF receptor, however, have not yet been characterized. We show that steroid hormones down‐regulate EGF‐induced tenascin‐C glycoprotein and its mRNA in these tenascin‐C‐non‐producing carcinoma cells. Of the steroids examined, hydrocortisone most effectively inhibited the secretion of tenascin‐C. These steroids did not affect EGF‐induced autophosphorylation or de novo synthesis of EGF receptors, nor did they compete for the binding of EGF to its receptor. Our results indicate that the induction of tenascin‐C by EGF and its down‐regulation by steroids might proceed in these carcinoma cells through separate signal transduction pathways. © 1995 Wiley‐Liss, Inc.
All Science Journal Classification (ASJC) codes
- Cancer Research