Dysregulation of the TGF-β Postreceptor＇Signaling Pathway in Cell Lines Derived from Primary or Metastatic Ovarian Cancer

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences 2004, Vol.24 (1), p.62-65
• Main Author: 奚玲 胡伟 孟力 周剑峰 卢运萍 王常玉 马丁
• Format: Article
• Language: English
• Subjects: Animals; cdc25 Phosphatases - metabolism; Cell Line, Tumor; DNA-Binding Proteins - metabolism; Female; Humans; Mice; Mice, Nude; Ovarian Neoplasms - metabolism; Ovarian Neoplasms - pathology; Proto-Oncogene Proteins c-myc - metabolism; Receptors, Transforming Growth Factor beta - metabolism; Signal Transduction; Smad4 Protein; Trans-Activators - metabolism; Transforming Growth Factor beta - pharmacology; 信号通道; 卵巢肿瘤; 细胞周期; 肿瘤转移; 转化生长因子-β
• ISSN: 1672-0733; 1993-1352

Transforming growth factor-beta (TGF-β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF-β. Mechanisms of resistance to TGF-β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF-β signaling transduction pathway such as C-myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF-β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C-myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi-quantitative RT-PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A genewas overexpressed with 88% (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20% (1/5) of non-tumorigenic cell lines (P