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Lack of transforming growth factor‐β type II receptor expression in human retinoblastoma cells
Author(s) -
Horie Kuniko,
Yamashita Hidetoshi,
Mogi Akira,
Takenoshita Seiichi,
Miyazono Kohei
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199806)175:3<305::aid-jcp8>3.0.co;2-s
Subject(s) - retinoblastoma , transfection , biology , microbiology and biotechnology , transforming growth factor , cell culture , gene , transforming growth factor beta , tgf beta signaling pathway , mutation , cancer research , genetics
Abstract Retinoblastoma cells are resistant to transforming growth factor‐β (TGF‐β) activity due to the absence of TGF‐β binding. To further elucidate the mechanism of TGF‐β resistance, we studied the expression of the TGF‐β receptors and SMADs by using the Y79 and WERI‐Rb‐1 retinoblastoma cell lines. Binding of 125 I‐TGF‐β1 to serine/threonine kinase receptor type II (TβR‐II) and TβR‐I was not seen in the retinoblastoma cells. TβR‐II mRNA was not expressed in these cells, but TβR‐I mRNA was detected. Mutation analysis revealed no mutation in the coding region of the TβR ‐II gene, and TβR‐II mRNA could be induced after the differentiation of Y79 cells. Smad2, Smad3, and Smad4, which are involved in TGF‐β signaling, were expressed in the retinoblastoma cells. Transcriptional activation of the TGF‐β‐responsive genes was not seen by the transfection of either recep‐tor cDNA alone but could be induced by transfection of both TβR‐II and TβR‐I. These data suggest that the defect in the TGF‐β response is caused by the lack of TβR‐II in the retinoblastoma cells. In addition, TβR‐I may be functionally inactivated in these cell lines. J. Cell. Physiol. 175:305–313, 1998. © 1998 Wiley‐Liss, Inc.