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

Journal Article · Fri Jul 21 00:00:00 EDT 2006 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2006.05.068· OSTI ID:20854363

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

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

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.

• OSTI ID: 20854363
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 346, 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); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

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