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  • American Association for Cancer Research (AACR)  (2)
  • Wang, Dong-Mei  (2)
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Publisher
  • American Association for Cancer Research (AACR)  (2)
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Language
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  • 1
    Online Resource
    Online Resource
    Insulin Receptor Substrate-1 Suppresses Transforming Growth Factor-β1–Mediated Epithelial-Mesenchymal Transition
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 18 ( 2009-09-15), p. 7180-7187
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 18 ( 2009-09-15), p. 7180-7187
    Abstract: We investigated the regulatory effect of insulin receptor substrate-1 (IRS-1) on transforming growth factor-β1 (TGF-β1)–induced epithelial-mesenchymal transition (EMT). TGF-β1–induced EMT and cell migration in A549 cells are associated with a decrease in IRS-1 tyrosine phosphorylation and protein levels. Tissue microarray analysis of human lung carcinoma shows a correlation between IRS-1 protein levels and E-cadherin protein levels. High IRS-1 levels coexist with high E-cadherin levels, whereas low IRS-1 levels coexist with low E-cadherin levels, implying a possibility that IRS-1 protein levels may be linked with EMT. Surprisingly, overexpression of IRS-1 in A549 cells completely blocked TGF-β1–induced EMT and cell migration, inhibited TGF-β1–mediated expression of snail and slug genes, and abolished TGF-β1–mediated repression of E-cadherin promoter activity. In contrast, IRS-1 knockdown by RNAi increased the expression of snail and slug genes and induced EMT. Inhibition of protein tyrosine phosphatase with sodium vanadate, which greatly increased the levels of tyrosine-phosphorylated IRS-1, suppressed TGF-β1–induced actin remodeling and cell morphologic changes. These results show for the first time that TGF-β1 induces EMT through mechanisms involving the modulation of IRS-1 signaling, and that IRS-1 functions as a critical EMT suppressor that suppresses TGF-β1–induced EMT via inhibition of snail and slug expression. [Cancer Res 2009;69(18):7180–7]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-08-4470
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Ferritin Heavy Chain–Mediated Iron Homeostasis and Subsequent Increased Reactive Oxygen Species Production Are Essential for Epithelial-Mesenchymal Transition
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 13 ( 2009-07-01), p. 5340-5348
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 13 ( 2009-07-01), p. 5340-5348
    Abstract: The epithelial-mesenchymal transition (EMT) plays a critical role in tumor progression. To obtain a broad view of the molecules involved in EMT, we carried out a comparative proteomic analysis of transforming growth factor-β1 (TGF-β1)–induced EMT in AML-12 murine hepatocytes. A total of 36 proteins with significant alterations in abundance were identified. Among these proteins, ferritin heavy chain (FHC), a cellular iron storage protein, was characterized as a novel modulator in TGF-β1–induced EMT. In response to TGF-β1, there was a dramatic decrease in the FHC levels, which caused iron release from FHC and, therefore, increased the intracellular labile iron pool (LIP). Abolishing the increase in LIP blocked TGF-β1–induced EMT. In addition, increased LIP levels promoted the production of reactive oxygen species (ROS), which in turn activated p38 mitogen-activated protein kinase. The elimination of ROS inhibited EMT, whereas H2O2 treatment rescued TGF-β1–induced EMT in cells in which the LIP increase was abrogated. Overexpression of exogenous FHC attenuated the increases in LIP and ROS production, leading to a suppression of EMT. We also showed that TGF-β1–mediated down-regulation of FHC occurs via 3′ untranslated region–dependent repression of the translation of FHC mRNA. Moreover, we found that FHC down-regulation is an event that occurs between the early and highly invasive advanced stages in esophageal adenocarcinoma and that depletion of LIP or ROS suppresses the migration of tumor cells. Our data show that cellular iron homeostasis regulated by FHC plays a critical role in TGF-β1–induced EMT. [Cancer Res 2009;69(13):5340–8]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-0112
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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