Nucleolin Promotes TGF-β Signaling Initiation via TGF-β Receptor I in Glioblastoma
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- 作者：Shunzeng Lv ; Jie Zhang ; Mingzhi Han ; Weiping Wang…
- 关键词：Nucleolin ; TGF ; β receptor I ; TGF ; β signaling ; Glioblastoma
- 刊名：Journal of Molecular Neuroscience
- 出版年：2015
- 出版时间：January 2015
- 年：2015
- 卷：55
- 期：1
- 页码：1-6
- 全文大小：1,374 KB
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- 出版者：Springer US
- ISSN：1559-1166
文摘
The transforming growth factor β (TGF-β) pathway plays a key role in oncogenesis of advanced cancers, involving the non-Smad and Smad pathways. Meanwhile, nucleolin on the cell surface has been also reported to affect activation of signaling pathways. However, the effect of cell surface nucleolin on TGF-β pathway in glioblastoma is not still understood. Here, using antibodies of nucleolin and TGF-β receptor I (TβR-I), we observed blocking of either nucleolin or TβR-I inhibited the phosphorylation of CrkL, Erk1/2, and Smad2. Using nucleolin siRNA, nucleolin knockdown was also identified to suppress the expression of p-CrkL, p-Erk1/2, and p-Smad2. Furthermore, immunoprecipitation revealed the interaction between cell surface nucleolin and TβR-I on the U87 cell membrane. In addition, U87 cell wound-healing, soft-agar and MTT assay also showed si-nucleolin could obviously impair wound closure (p--.001), colony formation (p--.001) and cell growth (p--.001). In conclusion, nucleolin promotes and regulates the TGF-β pathway by interacting with TβR-I and is required for initiation and activation of TGF-β signaling. Thus, nucleolin could be a key factor in glioblastoma pathogenesis and considered a therapeutic target, which may also mediate more signaling pathways.