Transforming Growth Factor β1 Suppresses Genomic Instability Independent of a G₁ Arrest, p53, and Rb (Cancer Research (1996) 56(16) (3645-3650))

Recently, it was brought to our auention that in our paper entitled “Trans forming Growth Factor β1 Suppresses Genomic Instability Independent of a G₁ Arrest, p53, and Rb” (Glick et al., Cancer Res., 56: 3645-3650, 1996), we incorrectly stated that Garrigue-Antar et al. (Cancer Res., 55: 3982-3987, 1995) reported a mutation in the TGF-β type II receptor in the TGF-β-resistant FaDu human carcinoma cell line, when it is actually wild type. This misstate ment does not alter the results of our study showing that FaDu cells do not respond to growth inhibition or suppression of PALA resistance by TGF-β. To determine the basis for nonresponsiveness to TGF-β, FaDu cells were transfected with the TGF-β response plasmid p800luc containing the PAl promoter (Abe et al., Anal. Biochem., 216: 276-284, 1994). TGF-β caused a 3-fold induction of luciferase activity in the control H4 mouse keratinocyte cell line, whereas there was no induction in either the FaDu cell line or the HCT1 16 colon carcinoma cell line, which contains a mutated TGF-β type II receptor (Fig. 1). This indicates that the lack of responsiveness to TGF-β in the FaDu cells is due to a defect in the TGF-β signaling pathway rather than other alterations indirectly affecting growth regulation by TGF-β. Addition ally, this suggests that the suppression of PALA resistance by TGF-β is linked to the signaling pathway regulating gene expression. We thank Dr. Michael Reiss for drawing our attention to the status of the TGF-β type II receptor in FaDu cells. (Figure presented.) Fig. I. FaDu cells are defective in the induction of gene expression by TGF-β. Triplicate wells were cotransfected with the plasmid p800Luc containing the TGF-β response element from the PAI promoter (Abe, et al., Anal. Biochem., 216: 276-284, 1994) and the internal control pRL-TK (Promega) and treated with I ng/ml TGF-β for 48 h. Luciferase activity was measured using the dual luciferase system (Promega), with luciferase activity from p800luc normalized to that obtained from pRL-TK. Similar results were obtained in two additional experiments. RLU, relative luciferase units.