Insulin action on H292 bronchial carcinoma cells as compared to normal bronchial epithelial cells.

Inhaled insulin may contribute to bronchial carcinoma due to IGF-I receptor activation by high local concentrations. Therefore, effects of insulin and IGF-I on human bronchial carcinoma cells (H292) and normal bronchial epithelium cells (HBE) were studied. TGF-β was included since it also influences carcinoma progression.