Retinoblastoma cells are resistant to transforming growth factor-b (TGF-b) activity due to the absence of TGF-b binding. To further elucidate the mechanism of TGF-b resistance, we studied the expression of the TGF-b receptors and SMADs by using the Y79 and WERI-Rb-1 retinoblastoma cell lines. Bindin
Dysregulated expression of transforming growth factor β and its type-I and type-II receptors in basal-cell carcinoma
✍ Scribed by Masutaka Furue; Mitsuyasu Kato; Koichiro Nakamura; Kiyoko Nashiro; Kanako Kikuchi; Hitoshi Okochi; Kohei Miyazono; Kunihiko Tamaki
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- French
- Weight
- 256 KB
- Volume
- 71
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
In mammals, transforming growth factor-beta (TGF-beta) is found in 3 highly homologous isoforms that exert their effects via heteromeric complexes of type-I and type-II receptors (TbetaR-I and TbetaR-II). TGF-beta regulates the growth and metabolism of various cell types, including keratinocytes. We have investigated the immunohistological localization of TGF-beta1, TGF-beta2, TbetaR-I and TbetaR-II in normal human skin, basal-cell carcinoma (BCC), Bowen's disease, seborrheic keratosis, eccrine poroma and eccrine spiradenoma using frozen tissue specimens. In normal human skin, the immunoreactive TGF-beta2, but not TGF-beta1, was detected predominantly in the epidermis, follicles and sebaceous glands. The epidermal expression of TbetaR-I and TbetaR-II was very weak in the majority of normal skins. In BCC, TGF-beta2 expression was markedly reduced or completely negative. In addition, TbetaR-I- and TbetaR-II-positive stromal cells were accumulated in the fibrotic stroma in some BCCs. These stromal cells were partly but moderately positive for TGF-beta1. Decreased expression of TGF-beta2 was likely to be associated with the differentiation state of BCC cells, since TGF-beta2 expression was clearly observed in the squamoid foci of BCC. In addition, no expression of TGF-beta2 was detected in the eccrine secretory portion or in eccrine spiradenoma, but it was detected in the upper eccrine ducts and in eccrine poroma.
📜 SIMILAR VOLUMES
To analyze transforming growth factor-b (TGF-b) response during MCF-7 cell progression, early passage (MCF-7E, õ200 passage) and late passage (MCF-7L, ú 500 passage) cells were compared. MCF-7E cells showed an IC 50 of Ç10 ng/ ml of TGF-b1, whereas MCF-7L cells were insensitive. MCF-7E cells contain
Alteration of transforming growth factor beta1 (TGF-beta1) type II receptor (RII) appears to cause unresponsiveness to TGF-beta1 in tumorigenic cells. Defect in the mononucleotide repeat sequence, i.e., poly A region of TGF-beta1RII gene has been reported to be related to replication error-positive
Fibroblasts play a critical role in wound repair and in the development of fibrotic diseases, and transforming growth factor-beta (TGF-beta) has been shown to profoundly modulate fibroblast function. However, there is limited information on the TGF-beta receptor types, isoform specificity, and compl
Transforming growth factor-b (TGF-b1) is a potent negative regulator of cell growth that transduces signals through interactions with type I and II receptors. Abnormal expression and mutational alterations of these receptors have been observed in several human malignancies. In this study, we investi
## Background: Resistance to the potent growth inhibitory effects of transforming growth factor-beta (tgf-beta) is a characteristic of many malignancies. tgf-beta insensitivity has been attributed to alterations in the number and function of the tgf-beta receptors as well as disturbances of downstr