Cellular growth inhibition by IGFBP-3 and TGF-β1 requires LRP-1

Shuan Shian Huang, Thai Yen Ling, Wen Fang Tseng, Yen Hwa Huang, Fen Mei Tang, Sandra M. Leal, Jung San Huang

研究成果: 雜誌貢獻文章

113 引文 (Scopus)

摘要

The type V TGF-β receptor (TβR-V)/ IGFBP-3 receptor mediates the IGF-independent growth inhibition induced by IGFBP-3. It also mediates the growth inhibitory response to TGF-β1 in concert with other TGF-β receptor types, and its loss may contribute to the malignant phenotype of human carcinoma cells. Here we demonstrate that TβR-V is identical to LRP-1/α2M receptor as shown by MALDI-TOF analysis of tryptic peptides of TβR-V purified from bovine liver. In addition, 125I-IGFBP-3 affinity-labeled TβR-V in Mv1Lu cells is immunoprecipitated by antibodies to LRP-1 and TβR-V. RAP, an LRP-1 antagonist, inhibits binding of 125I-TGF-β1 and 125I-IGFBP-3 to TβR-V and diminishes IGFBP-3-induced growth inhibition in Mv1Lu cells. Absent or low levels of LRP-1, as with TβR-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-β1 and IGFBP-3. LRP-1-deficient mouse embryonic fibroblasts lack a growth inhibitory response to TGF-β 1 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/TβR-V/IGFBP-3 receptor is required for the growth inhibitory response to IGFBP-3 and TGF-β1.

原文英語
頁(從 - 到)2068-2081
頁數14
期刊FASEB Journal
17
發行號14
DOIs
出版狀態已發佈 - 十一月 2003

指紋

Insulin-Like Growth Factor Binding Protein 3
insulin-like growth factor binding proteins
growth retardation
Growth
receptors
carcinoma
Cells
cells
Carcinoma
Phenotype
phenotype
Matrix-Assisted Laser Desorption-Ionization Mass Spectrometry
transfection
Fibroblasts
Liver
fibroblasts
Transfection
antagonists
Complementary DNA
lungs

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

引用此文

Huang, S. S., Ling, T. Y., Tseng, W. F., Huang, Y. H., Tang, F. M., Leal, S. M., & Huang, J. S. (2003). Cellular growth inhibition by IGFBP-3 and TGF-β1 requires LRP-1. FASEB Journal, 17(14), 2068-2081. https://doi.org/10.1096/fj.03-0256com

Cellular growth inhibition by IGFBP-3 and TGF-β1 requires LRP-1. / Huang, Shuan Shian; Ling, Thai Yen; Tseng, Wen Fang; Huang, Yen Hwa; Tang, Fen Mei; Leal, Sandra M.; Huang, Jung San.

於: FASEB Journal, 卷 17, 編號 14, 11.2003, p. 2068-2081.

研究成果: 雜誌貢獻文章

Huang, SS, Ling, TY, Tseng, WF, Huang, YH, Tang, FM, Leal, SM & Huang, JS 2003, 'Cellular growth inhibition by IGFBP-3 and TGF-β1 requires LRP-1', FASEB Journal, 卷 17, 編號 14, 頁 2068-2081. https://doi.org/10.1096/fj.03-0256com
Huang SS, Ling TY, Tseng WF, Huang YH, Tang FM, Leal SM 等. Cellular growth inhibition by IGFBP-3 and TGF-β1 requires LRP-1. FASEB Journal. 2003 11月;17(14):2068-2081. https://doi.org/10.1096/fj.03-0256com
Huang, Shuan Shian ; Ling, Thai Yen ; Tseng, Wen Fang ; Huang, Yen Hwa ; Tang, Fen Mei ; Leal, Sandra M. ; Huang, Jung San. / Cellular growth inhibition by IGFBP-3 and TGF-β1 requires LRP-1. 於: FASEB Journal. 2003 ; 卷 17, 編號 14. 頁 2068-2081.
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abstract = "The type V TGF-β receptor (TβR-V)/ IGFBP-3 receptor mediates the IGF-independent growth inhibition induced by IGFBP-3. It also mediates the growth inhibitory response to TGF-β1 in concert with other TGF-β receptor types, and its loss may contribute to the malignant phenotype of human carcinoma cells. Here we demonstrate that TβR-V is identical to LRP-1/α2M receptor as shown by MALDI-TOF analysis of tryptic peptides of TβR-V purified from bovine liver. In addition, 125I-IGFBP-3 affinity-labeled TβR-V in Mv1Lu cells is immunoprecipitated by antibodies to LRP-1 and TβR-V. RAP, an LRP-1 antagonist, inhibits binding of 125I-TGF-β1 and 125I-IGFBP-3 to TβR-V and diminishes IGFBP-3-induced growth inhibition in Mv1Lu cells. Absent or low levels of LRP-1, as with TβR-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-β1 and IGFBP-3. LRP-1-deficient mouse embryonic fibroblasts lack a growth inhibitory response to TGF-β 1 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/TβR-V/IGFBP-3 receptor is required for the growth inhibitory response to IGFBP-3 and TGF-β1.",
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AU - Huang, Shuan Shian

AU - Ling, Thai Yen

AU - Tseng, Wen Fang

AU - Huang, Yen Hwa

AU - Tang, Fen Mei

AU - Leal, Sandra M.

AU - Huang, Jung San

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N2 - The type V TGF-β receptor (TβR-V)/ IGFBP-3 receptor mediates the IGF-independent growth inhibition induced by IGFBP-3. It also mediates the growth inhibitory response to TGF-β1 in concert with other TGF-β receptor types, and its loss may contribute to the malignant phenotype of human carcinoma cells. Here we demonstrate that TβR-V is identical to LRP-1/α2M receptor as shown by MALDI-TOF analysis of tryptic peptides of TβR-V purified from bovine liver. In addition, 125I-IGFBP-3 affinity-labeled TβR-V in Mv1Lu cells is immunoprecipitated by antibodies to LRP-1 and TβR-V. RAP, an LRP-1 antagonist, inhibits binding of 125I-TGF-β1 and 125I-IGFBP-3 to TβR-V and diminishes IGFBP-3-induced growth inhibition in Mv1Lu cells. Absent or low levels of LRP-1, as with TβR-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-β1 and IGFBP-3. LRP-1-deficient mouse embryonic fibroblasts lack a growth inhibitory response to TGF-β 1 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/TβR-V/IGFBP-3 receptor is required for the growth inhibitory response to IGFBP-3 and TGF-β1.

AB - The type V TGF-β receptor (TβR-V)/ IGFBP-3 receptor mediates the IGF-independent growth inhibition induced by IGFBP-3. It also mediates the growth inhibitory response to TGF-β1 in concert with other TGF-β receptor types, and its loss may contribute to the malignant phenotype of human carcinoma cells. Here we demonstrate that TβR-V is identical to LRP-1/α2M receptor as shown by MALDI-TOF analysis of tryptic peptides of TβR-V purified from bovine liver. In addition, 125I-IGFBP-3 affinity-labeled TβR-V in Mv1Lu cells is immunoprecipitated by antibodies to LRP-1 and TβR-V. RAP, an LRP-1 antagonist, inhibits binding of 125I-TGF-β1 and 125I-IGFBP-3 to TβR-V and diminishes IGFBP-3-induced growth inhibition in Mv1Lu cells. Absent or low levels of LRP-1, as with TβR-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-β1 and IGFBP-3. LRP-1-deficient mouse embryonic fibroblasts lack a growth inhibitory response to TGF-β 1 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/TβR-V/IGFBP-3 receptor is required for the growth inhibitory response to IGFBP-3 and TGF-β1.

KW - Carcinogenesis

KW - Epithelial cells

KW - Growth inhibition

KW - IGFBP-3 receptor

KW - Type V TGF-β receptor

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