PKB negatively modulates TGF-β responsiveness in prostate carcinoma PC-3 cells through its interaction with Smad3

LI Wei; XIN Dianqi; GUO Yinlu

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PKB negatively modulates TGF-β responsiveness in prostate carcinoma PC-3 cells through its interaction with Smad3

机译：PKB通过与Smad3的相互作用负调节前列腺癌PC-3细胞中的TGF-β反应。

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Most prostate cancers are insensitive to growth-inhibitory effect of TGF-β, while PI3K-PKB signaling is highly activated in prostate cancers. We investigated whether the PI3K-PKB signaling contributes to TGF-β insensitivity in PTEN-null prostate cancer PC-3 cells. Cell growth analysis showed that inhibition of PI3K-PKB pathway by LY294002 enhanced growth inhibition and cell cycle arrest induced by TGF-β. Furthermore, activation of PI3K-PKB pathway by insulin or overexpression of PKB decreased the transcriptional activity of TGF-β, as measured by the TGF-β/Smad3-responsive CAGA-luciferase reporter, while inhibition of PI3K-PKB pathway by introducing PTEN, inactive PKB mutant or using LY294002 promoted TGF-β-induced expression of CAGA-luciferase. Co-immunoprecipitation studies further demonstrated that Smad3 interacted with PKB through its linker region and MH2 domain. This interaction was facilitated by insulin and disrupted by TGF-β signaling activation. Our results suggest that the PI3K-PKB pathway may play an important role in rendering cell resistance to the antiproliferative effect of TGF-β and regulating cell response to TGF-β.

机译：大多数前列腺癌对TGF-β的生长抑制作用不敏感，而PI3K-PKB信号在前列腺癌中被高度激活。我们调查了PI3K-PKB信号是否有助于PTEN无效的前列腺癌PC-3细胞中的TGF-β不敏感。细胞生长分析表明，LY294002抑制PI3K-PKB通路可增强TGF-β诱导的生长抑制和细胞周期阻滞。此外，由TGF-β/ Smad3响应的CAGA-萤光素酶报告基因测定，胰岛素激活PI3K-PKB途径或PKB过度表达会降低TGF-β的转录活性，而通过引入PTEN抑制PI3K-PKB途径，无活性的PKB突变体或使用LY294002可以促进TGF-β诱导的CAGA荧光素酶表达。免疫共沉淀研究进一步表明，Smad3通过其接头区和MH2结构域与PKB相互作用。胰岛素促进了这种相互作用，而TGF-β信号激活则破坏了这种相互作用。我们的结果表明，PI3K-PKB途径可能在使细胞抵抗TGF-β的抗增殖作用和调节细胞对TGF-β的反应中起重要作用。

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来源
《Chinese science bulletin》 |2006年第13期|p.1563-1570|共8页
作者
LI Wei; XIN Dianqi; GUO Yinlu;
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作者单位

Department of Urology, the First Hospital of Peking University;

the Urological Research Institute, Peking University, Beijing 100034, China;

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原文格式 PDF
正文语种 eng
中图分类自然科学现状及发展;
关键词
prostate carcinoma; protein kinase B; transforming growth factor beta; Smad3; protein interaction;

机译：前列腺癌;蛋白激酶B;转化生长因子β;Smad3;蛋白相互作用;

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专利

1. PKB negatively modulates TGF-beta responsiveness in prostate carcinoma PC-3 cells through its Interaction with Smad3 [J] . LI Wei, XIN Dianqi, GUO Yinlu Chinese science bulletin . 2006,第13期

机译：PKB通过与Smad3的相互作用负调节前列腺癌PC-3细胞中的TGF-β反应。
2. PKB negatively modulates TGF-p responsiveness in prostate carcinoma PC-3 cells through its interaction with Smad3 [J] . LI Wei, XIN Dianqi, QUO Yinlu Chinese science bulletin . 2006,第13期

机译：PKB通过与Smad3的相互作用负调节前列腺癌PC-3细胞中的TGF-p反应性
3. PKB/Akt modulates TGF-β signalling through a direct interaction with Smad3 [J] . Ingrid Remy, Annie Montmarquette, Stephen W. Michnick Nature cell biology . 2004,第4期

机译：PKB / Akt通过与Smad3的直接相互作用调节TGF-β信号传导
4. Characterization of the Secretome of Vascular Smooth Muscle Cells in Response to TGF-β/Smad3 by Label-free MS~E Quantication [C] . Chenxi Yang, Di Ma, Xudong Shi, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2013

机译：血管平滑肌细胞克切术响应于TGF-β/ Smad3的无标记MS〜e量化表征
5. Regulation of prostatic carcinoma cells (DU145) by bone growth factors using co-cultures of osteoblast and prostate carcinoma cells across a fabricated collagen matrix. [D] . Macias, Chanda Latrice. 2001

机译：使用成骨细胞和前列腺癌细胞在人造胶原基质上的共培养物，通过骨生长因子调节前列腺癌细胞（DU145）。
6. DHT Selectively Reverses Smad3-Mediated/TGF-β-Induced Responses through Transcriptional Down-Regulation of Smad3 in Prostate Epithelial Cells [O] . Kyung Song, Hui Wang, Tracy L. Krebs, -1

机译：DHT通过转录上调Smad3在前列腺上皮细胞中选择性逆转Smad3介导的/TGF-β诱导的反应。
7. Suppression of Constitutive and Tumor Necrosis Factor α-Induced Nuclear Factor (NF)-κB Activation and Induction of Apoptosis by Apigenin in Human Prostate Carcinoma PC-3 Cells: Correlation with Down-Regulation of NF-κB-Responsive Genes [O] . Sanjeev Shukla, Sanjay Gupta 2004

机译：抑制组成型和肿瘤坏死因子α-诱导的核因子（NF）-κB活化和诱导人类前列腺癌PC-3细胞凋亡的诱导：与NF-κB反应基因的下调相关性

PKB negatively modulates TGF-β responsiveness in prostate carcinoma PC-3 cells through its interaction with Smad3

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