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.
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Authors | Motoyoshi Tanaka, H Barton Grossman |
Journal | Oncology reports
(Oncol Rep)
Vol. 11
Issue 2
Pg. 537-41
(Feb 2004)
ISSN: 1021-335X [Print] Greece |
PMID | 14719096
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Antineoplastic Agents
- Connexins
- GJB2 protein, human
- Proto-Oncogene Proteins c-bcl-2
- Connexin 26
- Doxorubicin
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Topics |
- 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)
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