Connexin 26 induces growth suppression, apoptosis and increased efficacy of doxorubicin in prostate cancer cells

Oncol Rep. 2004 Feb;11(2):537-41.

Abstract

Connexin 26 (Cx26) encodes a gap junction protein and is a putative tumor suppressor gene. We evaluated the effect of forced expression of Cx26 on three human prostate cancer cell lines, PC-3, LNCap, and DU-145. The three cell lines were infected with a Cx26 adenovirus vector (Ad-Cx26) or a control vector or were mock infected. We tested cell growth, cell cycle, apoptosis, and the efficacy of combined treatment with doxorubicin. Ad-Cx26 infection suppressed the growth of all the cell lines compared with controls and induced cell cycle arrest at the G2/M phase and apoptosis. Ad-Cx26 decreased the expression of Bcl-2. LNCaP cell growth was dramatically suppressed by Ad-Cx26 alone. PC-3 and DU-145 had greater growth suppression with combined gene therapy and chemotherapy than with either Ad-Cx26 or doxorubicin alone. Forced expression of Cx26 suppresses the growth of prostate cancer cells and decreases the expression of Bcl-2. Combining Cx26 gene therapy with doxorubicin results in greater growth suppression.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antineoplastic Agents / toxicity
  • Apoptosis / physiology*
  • Cell Division / physiology*
  • Cell Line, Tumor
  • Connexin 26
  • Connexins / physiology*
  • Doxorubicin / toxicity*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Genetic Therapy
  • Humans
  • Male
  • Prostatic Neoplasms
  • Proto-Oncogene Proteins c-bcl-2 / genetics

Substances

  • Antineoplastic Agents
  • Connexins
  • GJB2 protein, human
  • Proto-Oncogene Proteins c-bcl-2
  • Connexin 26
  • Doxorubicin