Log in

Role of decay-accelerating factor in regulating survival of human cervical cancer cells

  • Original Paper
  • Published:
Journal of Cancer Research and Clinical Oncology Aims and scope Submit manuscript

Abstract

Background

Decay-accelerating factor (DAF) is one of the key molecules involved in cell protection against autologous complement, which restricts the action of complement at critical stages of the cascade reaction. The effect of DAF on the survival of human cervical cancer cell (ME180) has not been demonstrated.

Methods

In this study we applied, for the first time, small interference RNA (siRNA) to knock down the expression of the DAF with the aim of exploiting complement more effectively for tumor cell damage. Meanwhile, we investigated the effects of DAF on the viability and migration, moreover the proliferation of ME180 cell.

Results

The results showed that the expression of DAF was significantly increased in human cervical cancer tissues. SiRNA inhibition of DAF expression enhanced complement-dependent cytolysis up to 32% in ME180 cells, which contributed to the control of C3 activation and increased the cells viability, migration and augment the number of ME180 cells.

Conclusion

These data indicated that DAF siRNA described in this study may offer an additional alternative to improve the efficacy of antibody- and complement-based cancer immunotherapy.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Subscribe and save

Springer+ Basic
EUR 32.99 /Month
  • Get 10 units per month
  • Download Article/Chapter or Ebook
  • 1 Unit = 1 Article or 1 Chapter
  • Cancel anytime
Subscribe now

Buy Now

Price includes VAT (France)

Instant access to the full article PDF.

Fig. 1
Fig. 2
Fig. 3
Fig. 4

Similar content being viewed by others

References

  • Andersson S, Hellstr AC, Ren ZP et al (2006) The carcinogenic role of oncogenic HPV and p53 gene mutation in cervical adenocarcinomas. Med Oncol 23:113–119

    Article  CAS  PubMed  Google Scholar 

  • Arora M, Arora R, Tiwari SC et al (2000) Expression of complement regulatory proteins in diffuse proliferative glomerulonephritis. Lupus 9:127–131

    Article  CAS  PubMed  Google Scholar 

  • Bjorge L, Hakulinen J, Wahlstrom T et al (1997) Complement-regulatory proteins in ovarian malignancies. Int J Cancer 70:14–25

    Article  CAS  PubMed  Google Scholar 

  • Bosch FX, Sanjose S (2003) Human papillomavirus and cervical cancer-burden and assessment of causality. J Natl Cancer Inst Monogr 31:3–13

    PubMed  Google Scholar 

  • Castellsague X, Diaz M, Sanjose S et al (2006) Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. J Natl Cancer Inst 98:303–315

    Article  PubMed  Google Scholar 

  • Cole DS, Morgan BP (2003) Beyond lysis: how complement influences cell fate. Clin Sci 104:455–466

    Article  CAS  PubMed  Google Scholar 

  • García VI, Atisha FY, Richaud PY et al (2006) Diminished expression of complement regulatory proteins (CD55 and CD59) in lymphocytes from systemic lupus erythematosus patients with lymphopenia. Lupus 15:600–605

    Article  Google Scholar 

  • His BL, Hunt JS, Atkinson JP et al (1991) Differential expression of complement regulatory proteins on subpopulations of human trophoblast cells. J Reprod Immunol 19:209–223

    Article  Google Scholar 

  • Holmes CH, Simpson KL, Wainwright SD et al (1990) Preferential expression of the complement regulatory protein decay accelerating factor at the fetomaternal interface during human pregnancy. J Immunol 144:3099–3105

    CAS  PubMed  Google Scholar 

  • Jemal A, Siegel R, Ward E et al (2006) Cancer statistics. J Clin 56:106–130

    Google Scholar 

  • Kiso T, Mizuno M, Nasu J et al (2002) Enhanced expression of decay-accelerating factor and CD59/homologous restriction factor 20 in intestinal metaplasia, gastric adenomas and intestinal-type gastric carcinomas but not in diffuse-type carcinomas. Histopathology 40:339–347

    Article  CAS  PubMed  Google Scholar 

  • Li L, Spendlove I, Morgan J et al (2001) CD55 is over-expressed in the tumour environment. Br J Cancer 84:80–86

    Article  CAS  PubMed  Google Scholar 

  • Parkin DM, Bray F, Ferlay J et al (2001) Estimating the world cancer burden: Globocan 2000. Int J Cancer 94:153–156

    Article  CAS  PubMed  Google Scholar 

  • Richaud PY, Pérez RB, Carrillo ME et al (2003) Deficiency of red cell bound CD55 and CD59 in patients with systemic lupus erythematosus. Immunol Lett 88:95–99

    Article  Google Scholar 

  • Van BJ, Van MM, Hart BA et al (2005) Decay-accelerating factor (CD55) is expressed by neurons in response to chronic but not acute autoimmune central nervous system inflammation associated with complement activation. J Immunol 174:2353–2365

    Google Scholar 

  • Zell S, Geis N, Rutz R et al (2007) Down-regulation of CD55 and CD46 expression bu anti-sense phosphorothioate oligonucleotides (S-ODNs) sensitizes tumour cells to complement attack. Clin Exp Immunol 150:576–584

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgments

The study was supported in part by Nan**g Medical University Natural Science Foundation (No.08NMUZ031) and Nan**g Health Bureau Medical Science Foundation (No. YKK08112).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to **-Qing Gu.

Additional information

The authors L.-J. Gao and L. Ding contributed equally to this work.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary material 1 (PDF 42 kb)

Rights and permissions

Reprints and permissions

About this article

Cite this article

Gao, LJ., Ding, L., Guo, SY. et al. Role of decay-accelerating factor in regulating survival of human cervical cancer cells. J Cancer Res Clin Oncol 137, 81–87 (2011). https://doi.org/10.1007/s00432-010-0862-3

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00432-010-0862-3

Keywords

Navigation