[Effects of transforming growth factor-beta/Smad signaling on the growth and apoptosis of human rhabdomyosarcoma cell line RD]

Zhonghua Bing Li Xue Za Zhi. 2005 Jul;34(7):407-12.
[Article in Chinese]

Abstract

Objective: To study the effects of TGF-beta/Smad signaling on the growth and apoptosis of human rhabdomyosarcoma cell line RD.

Methods: Biosynthesized short hairpin RNA (shRNA) was transfected into RD cells by cation liposome vector to suppress Smad4 expression. The mRNA and protein expression of Smad4 in RD after shRNA-transfection were examined by RT-PCR and Western blot respectively. Immunofluorescent staining was used to detect the location of Smad2/3 in RD by laser scanning confocal microscopy. The viability of RD cells was examined by MTT method and (3)H-thymidine incorporation assay. The apoptosis of RD was examined by flow cytometry analysis and fluorescent staining.

Results: The expression of mRNA and protein of Smad4 in RD were effectively suppressed by shRNA interference. Such suppression effectively interrupted the endogenous TGF-beta/Smad signaling and consequently blocked the translocation of Smad2/3. The interruption of endogenous TGF-beta/Smad signaling not only inhibited the growth of RD but also induced apoptosis of RD. Exogenous TGF-beta1 inhibited the growth of RD but did not influence the apoptosis of RD.

Conclusion: shRNA interference can effectively interrupt the TGF-beta/Smad signaling by suppressing the expression of Smad4. TGF-beta/Smad signaling subtly regulates the growth and apoptosis of RD.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Cell Nucleus / metabolism
  • Cell Proliferation / drug effects
  • Cytoplasm / metabolism
  • Humans
  • Protein Transport
  • RNA Interference*
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • RNA, Small Interfering / pharmacology
  • Rhabdomyosarcoma / genetics
  • Rhabdomyosarcoma / metabolism
  • Rhabdomyosarcoma / pathology*
  • Signal Transduction
  • Smad2 Protein / metabolism
  • Smad3 Protein / metabolism
  • Smad4 Protein / biosynthesis*
  • Smad4 Protein / genetics
  • Transfection
  • Transforming Growth Factor beta1 / pharmacology*

Substances

  • RNA, Messenger
  • RNA, Small Interfering
  • SMAD2 protein, human
  • Smad2 Protein
  • Smad3 Protein
  • Smad4 Protein
  • Transforming Growth Factor beta1