RhoC is essential for TGF-{beta}1-induced invasive capacity of rat ascites hepatoma cells

Mukai, M; Endo, H; Iwasaki, T; Tatsuta, M; Togawa, A; Nakamura, H; Inoue, M

doi:10.1016/j.bbrc.2006.05.068

Title: RhoC is essential for TGF-{beta}1-induced invasive capacity of rat ascites hepatoma cells

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Abstract

Transforming growth factor-{beta}1 (TGF-{beta}1) is a multifunctional growth factor that plays a role in cell proliferation, differentiation, extracellular matrix production, apoptosis, and cell motility. We show here that TGF-{beta}1 increased the invasiveness of MM1 cells, which are a highly invasive clone of rat ascites hepatoma cells. Both mRNA and protein levels of RhoC but not RhoA in TGF-{beta}1-treated MM1 cells increased. In parallel with this increase in expression, RhoC activity was induced by TGF-{beta}1 treatment. When RhoC was overexpressed in MM1 cells, the invasive capacity increased. The RhoC-overexpressing cells formed more nodules than did mock cells when injected into rat peritoneum. Furthermore, when RhoC expression was reduced by transfection with shRNA/RhoC, the invasiveness of MM1 cells decreased with concomitant suppression of RhoC expression. Thus, the induced expression of RhoC by TGF-{beta}1 in MM1 cells plays a critical role in TGF-{beta}1-induced cell migration.

Authors:

Mukai, M ^[1]; Endo, H ^[1]; Iwasaki, T ^[2]; Tatsuta, M ^[3]; Togawa, A ^[4]; Nakamura, H ^[1]; Inoue, M ^[1]

Department of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka 537-8511 (Japan)
Department of Respiratory Surgery, Osaka Prefectural Medical Center for Respiratory and Allergic Diseases, Osaka 583-8588 (Japan)
Department of Gastrointestinal Oncology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka 537-8511 (Japan)
RIKEN Center for Developmental Biology, Laboratory for Stem Cell Research, Kobe 650-0047 (Japan)

Publication Date:: Fri Jul 21 00:00:00 EDT 2006

OSTI Identifier:: 20854363

Resource Type:: Journal Article

Journal Name:: Biochemical and Biophysical Research Communications

Additional Journal Information:: Journal Volume: 346; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2006.05.068; PII: S0006-291X(06)01126-0; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; APOPTOSIS; ASCITES; CELL PROLIFERATION; GROWTH FACTORS; HEPATOMAS; INHIBITION; PERITONEUM; RATS

Citation Formats


                    Mukai, M, Endo, H, Iwasaki, T, Tatsuta, M, Togawa, A, Nakamura, H, and Inoue, M. RhoC is essential for TGF-{beta}1-induced invasive capacity of rat ascites hepatoma cells.  United States: N. p., 2006. 
        Web.  doi:10.1016/j.bbrc.2006.05.068.

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                    Mukai, M, Endo, H, Iwasaki, T, Tatsuta, M, Togawa, A, Nakamura, H, & Inoue, M. RhoC is essential for TGF-{beta}1-induced invasive capacity of rat ascites hepatoma cells.  United States.  https://doi.org/10.1016/j.bbrc.2006.05.068

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                    Mukai, M, Endo, H, Iwasaki, T, Tatsuta, M, Togawa, A, Nakamura, H, and Inoue, M. 2006.  
        "RhoC is essential for TGF-{beta}1-induced invasive capacity of rat ascites hepatoma cells".  United States.  https://doi.org/10.1016/j.bbrc.2006.05.068.

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@article{osti_20854363,

  title        = {RhoC is essential for TGF-{beta}1-induced invasive capacity of rat ascites hepatoma cells},

  author       = {Mukai, M and Endo, H and Iwasaki, T and Tatsuta, M and Togawa, A and Nakamura, H and Inoue, M},

  abstractNote = {Transforming growth factor-{beta}1 (TGF-{beta}1) is a multifunctional growth factor that plays a role in cell proliferation, differentiation, extracellular matrix production, apoptosis, and cell motility. We show here that TGF-{beta}1 increased the invasiveness of MM1 cells, which are a highly invasive clone of rat ascites hepatoma cells. Both mRNA and protein levels of RhoC but not RhoA in TGF-{beta}1-treated MM1 cells increased. In parallel with this increase in expression, RhoC activity was induced by TGF-{beta}1 treatment. When RhoC was overexpressed in MM1 cells, the invasive capacity increased. The RhoC-overexpressing cells formed more nodules than did mock cells when injected into rat peritoneum. Furthermore, when RhoC expression was reduced by transfection with shRNA/RhoC, the invasiveness of MM1 cells decreased with concomitant suppression of RhoC expression. Thus, the induced expression of RhoC by TGF-{beta}1 in MM1 cells plays a critical role in TGF-{beta}1-induced cell migration.},

  doi          = {10.1016/j.bbrc.2006.05.068},

  url          = {https://www.osti.gov/biblio/20854363},
  journal      = {Biochemical and Biophysical Research Communications},

  issn         = {0006-291X},

  number       = 1,

  volume       = 346,

  place        = {United States},

  year         = {Fri Jul 21 00:00:00 EDT 2006},

  month        = {Fri Jul 21 00:00:00 EDT 2006}

}

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