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论文题目: MicroRNA-182 targets SMAD7 to potentiate TGF beta-induced epithelial-mesenchymal transition and metastasis of cancer cells
英文论文题目: MicroRNA-182 targets SMAD7 to potentiate TGF beta-induced epithelial-mesenchymal transition and metastasis of cancer cells
第一作者: Yu, JY; Lei, R; Zhuang, XQ; Li, XX; Li, G; Lev, S; Segura, MF; Zhang, X; Hu, GH
英文第一作者: Yu, JY; Lei, R; Zhuang, XQ; Li, XX; Li, G; Lev, S; Segura, MF; Zhang, X; Hu, GH
联系作者: Hu, GH (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai 200031, Peoples R China.
英文联系作者: Hu, GH (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai 200031, Peoples R China.
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发表年度: 2016
卷: 7
期:
页码: 13884
摘要: The transforming growth factor beta (TGF beta) pathway plays critical roles during cancer cell epithelial-mesenchymal transition (EMT) and metastasis. SMAD7 is both a transcriptional target and a negative regulator of TGF beta signalling, thus mediating a negative feedback loop that may potentially restrain TGF beta responses of cancer cells. Here, however, we show that TGFb treatment induces SMAD7 transcription but not its protein level in a panel of cancer cells. Mechanistic studies reveal that TGFb activates the expression of microRNA-182 (miR-182), which suppresses SMAD7 protein. miR-182 silencing leads to SMAD7 upregulation on TGF beta treatment and prevents TGF beta-induced EMT and invasion of cancer cells. Overexpression of miR-182 promotes breast tumour invasion and TGFb-induced osteoclastogenesis for bone metastasis. Furthermore, miR-182 expression inversely correlates with SMAD7 protein in human tumour samples. Therefore, our data reveal the miR-182-mediated disruption of TGF beta self-restraint and provide a mechanism to explain the unleashed TGF beta responses in metastatic cancer cells.
英文摘要: The transforming growth factor beta (TGF beta) pathway plays critical roles during cancer cell epithelial-mesenchymal transition (EMT) and metastasis. SMAD7 is both a transcriptional target and a negative regulator of TGF beta signalling, thus mediating a negative feedback loop that may potentially restrain TGF beta responses of cancer cells. Here, however, we show that TGFb treatment induces SMAD7 transcription but not its protein level in a panel of cancer cells. Mechanistic studies reveal that TGFb activates the expression of microRNA-182 (miR-182), which suppresses SMAD7 protein. miR-182 silencing leads to SMAD7 upregulation on TGF beta treatment and prevents TGF beta-induced EMT and invasion of cancer cells. Overexpression of miR-182 promotes breast tumour invasion and TGFb-induced osteoclastogenesis for bone metastasis. Furthermore, miR-182 expression inversely correlates with SMAD7 protein in human tumour samples. Therefore, our data reveal the miR-182-mediated disruption of TGF beta self-restraint and provide a mechanism to explain the unleashed TGF beta responses in metastatic cancer cells.
刊物名称: NATURE COMMUNICATIONS
英文刊物名称: NATURE COMMUNICATIONS
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学科: Multidisciplinary Sciences
英文学科: Multidisciplinary Sciences
影响因子: 12.124
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论文类别: Article
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