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* Departments of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, Missouri, USA;
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; and
Department of Biochemistry, Taipei Medical University, Taipei, Taiwan
1 Correspondence: Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, 1402 South Grand Blvd., St. Louis, MO 63104, USA. E-mail: huangss{at}slu.edu or huangjs{at}slu.edu
The type V TGF-ß receptor (TßR-V)/IGFBP-3 receptor mediates the IGF-independent growth inhibition induced by IGFBP-3. It also mediates the growth inhibitory response to TGF-ß1 in concert with other TGF-ß receptor types, and its loss may contribute to the malignant phenotype of human carcinoma cells. Here we demonstrate that TßR-V is identical to LRP-1/
2M receptor as shown by MALDI-TOF analysis of tryptic peptides of TßR-V purified from bovine liver. In addition, 125I-IGFBP-3 affinity-labeled TßR-V in Mv1Lu cells is immunoprecipitated by antibodies to LRP-1 and TßR-V. RAP, an LRP-1 antagonist, inhibits binding of 125I-TGF-ß1 and 125I-IGFBP-3 to TßR-V and diminishes IGFBP-3-induced growth inhibition in Mv1Lu cells. Absent or low levels of LRP-1, as with TßR-V, have been linked to the malignant phenotype of carcinoma cells. Mutagenized Mv1Lu cells selected for reduced expression of LRP-1 have an attenuated growth inhibitory response to TGF-ß1 and IGFBP-3. LRP-1-deficient mouse embryonic fibroblasts lack a growth inhibitory response to TGF-ß1 and IGFBP-3. On the other hand, stable transfection of H1299 human lung carcinoma cells with LRP-1 cDNA restores the growth inhibitory response. These results suggest that the LRP-1/TßR-V/IGFBP-3 receptor is required for the growth inhibitory response to IGFBP-3 and TGF-ß1.—Huang, S. S., Ling, T.-Y., Tseng, W.-F., Huang, Y.-H., Tang, F.-M., Leal, S. M., Huang, J. S. Cellular growth inhibition by IGFBP-3 and TGF-ß1 requires LRP-1.
Key Words: type V TGF-ß receptor • IGFBP-3 receptor • growth inhibition • epithelial cells • carcinogenesis
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