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Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3.

Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3. Research Abstract Details 

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  • Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3. Abstract Text:

    yanan yangYanan Yang,xinchao panXinchao Pan,weiwei leiWeiwei Lei,jun wangJun Wang,jian shiJian Shi,fuqiang liFuqiang Li,jianguo songJianguo Song,

    Apoptosis and epithelial-to-mesenchymal transdifferentiation or transition (EMT) are crucial for normal development and body homeostasis. The alterations of these events are closely related to some pathologic processes, such as tumor formation and metastasis, fibrotic diseases of liver and kidney, and abnormal development of embryos. The mechanism that underlies the simultaneously occurring apoptosis and EMT induced by transforming growth factor-beta (TGF-beta) has not been well studied. In this report, we investigated the potential mechanism that underlies TGF-beta1-induced apoptosis and EMT. TGF-beta1-induced apoptosis and EMT were associated with the activation of protein kinase A (PKA) and signal transducers and activators of transcription 3 (STAT3). Inhibition of PKA by specific PKA inhibitor H89 or by PKA inhibitor peptide blocked STAT3 activation and suppressed TGF-beta1-induced apoptosis and EMT. Furthermore, overexpression of a phosphorylation-deficient form of STAT3, but not wild-type STAT3, produced an inhibitory effect on TGF-beta1-induced apoptosis and EMT. The results indicate that PKA is an upstream regulator for TGF-beta1-induced STAT3 activation and plays an important role in TGF-beta1-mediated apoptosis and EMT. These studies provided a new insight into the signaling mechanism underlying the apoptosis and EMT, which could be of importance in understanding some related physiologic and pathologic processes.

    Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3. Publishing Authors By Initials

    y yangY Yang,x panX Pan,w leiW Lei,j wangJ Wang,j shiJ Shi,f liF Li,j songJ Song,

    For similar abstracts research abstracts see: abstracts research

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    Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Cancer research

    VOLUME: 66

    Page Numbers: 8617-24

    Journal Abbreviation:

    ISSN: 1538-7445

    DAY: 1

    MONTH: Sep

    YEAR: 2006

    Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3. Information

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    LANGUAGE: eng

    NlmUniqueID: 2984705

    Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3. Keywords Mesh Terms:

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    Grant and Affiliation Information for Regulation of transforming growth factor-beta 1-induced apoptosis and epithelial-to-mesenchymal transition by protein kinase A and signal transducers and activators of transcription 3.

    AFFILIATION: Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Cancer Res

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