Sequential effects of the proteasome inhibitor bortezomib and chemotherapeutic agents in uterine cervical cancer cell lines

Oncol Rep. 2013 Jan;29(1):51-7. doi: 10.3892/or.2012.2072. Epub 2012 Oct 5.

Abstract

Although the prognosis of uterine cervical cancer has improved due to the advances of treatment modalities, survival of recurrent or metastatic cervical cancer remains poor. Cisplatin is an effective radiosensitizer, but its single agent activity in recurrent cervical cancer is disappointing. Inactivation of tumor suppressors through ubiquitin-mediated degradation by human papillomavirus is known to be a critical step in the carcinogenesis of uterine cervix. Bortezomib, a selective inhibitor of the proteasome, has been shown to inhibit the growth of several solid tumors. To determine the role of bortezomib in cervical cancer as a chemotherapeutic agent, we studied its biological properties. Bortezomib efficiently inhibited the proteasomal activities in cervical cancer cells, and an increased expression of tumor suppressors such as p53, hDlg and hScrib became evident. In addition, sequential or concomitant treatment of bortezomib and cisplatin stimulated the expression of p53, hScrib and p21 and the stimulation was markedly influenced by the order of drugs in HeLa cells. We further confirmed that the concomitant use of bortezomib and cisplatin has synergistic inhibitory effects on the growth of xenograft tumors derived from HeLa cells. Our data establish the possibility that the concomitant use of bortezomib and cisplatin could be an alternative choice in cases resistant to conventional chemotherapy, and sequential effects must be considered for advanced and therapy-resistant cervical cancer patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Apoptosis / drug effects*
  • Blotting, Western
  • Boronic Acids / administration & dosage
  • Bortezomib
  • Carboplatin / administration & dosage
  • Cell Proliferation / drug effects*
  • Cisplatin / administration & dosage
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Drug Synergism*
  • Female
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Humans
  • Membrane Proteins / metabolism
  • Mice
  • Mice, Inbred ICR
  • Mice, SCID
  • Paclitaxel / administration & dosage
  • Pyrazines / administration & dosage
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins / metabolism
  • Uterine Cervical Neoplasms / drug therapy*
  • Uterine Cervical Neoplasms / metabolism
  • Uterine Cervical Neoplasms / pathology

Substances

  • Boronic Acids
  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Membrane Proteins
  • Pyrazines
  • SCRIB protein, human
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • Bortezomib
  • Carboplatin
  • Paclitaxel
  • Cisplatin