TSH is the classic stimulator of thyroid cell function. Clinically, treatment with thyroxin to suppress TSH decreased the risk of thyroid cancer recurrence and improved patient survival. This study analyzed the effect of stably transfected human TSH receptor cDNA in an established model of metastatic follicular thyroid cancer cells (FC) compared to wild type FTC. Wild type FTC lack TSH receptors and do not depend on TSH for growth. However, they contain thyroglobulin, have intact thyroid functions and response to TSH. We tested growth, invasion, and adhesion of transfected tumor cells (FTC-TSHr) compared to parental cells. All transfected FTC-TSHr expressed TSHr mRNA. Compared to wild type cells invasion and growth of TSHr-transfected FTC were significantly inhibited (p < 0.001). All FTC adhered best to collagen IV and fibronectin. Compared to parental cells adhesion of unstimulated FTC-TSHr was significantly enhanced (p < 0.001). These in vitro data underline the important role of the human TSH receptor as the main regulator of thyroid growth and functions.