Expression of cell-cycle mediators in ovarian cancer cells after transfection with p16(INK4a), p21(WAF1/Cip-1), and p53.
Gynecol Oncol
; 83(3): 543-8, 2001 Dec.
Article
en En
| MEDLINE
| ID: mdl-11733969
OBJECTIVE: The purpose of this study was to determine whether transfection of ovarian cancer cell lines with recombinant adenoviral vectors containing wild-type p16(INK4a), p21(WAF1/Cip-1), and p53 caused growth inhibition and induction of apoptosis. We also measured the expression of the cell-cycle mediators Bax, Bcl-2, pRb, and mdm-2. METHODS: We introduced the wild-type p16(INK4a), p21(WAF1/Cip-1), and p53 genes into the ovarian cancer cell lines SK-OV-3 (p16(INK4a) and p53 null) and OVCA-420 (p16(INK4a) and p53 wild-type) by adenoviral transfection. Cell growth inhibition was measured over a 10-day period. Induction of apoptosis was tested for both cell lines 48 h after cell transfection. Expression of cell-cycle mediators was evaluated by Western blot analysis and densitometry. RESULTS: Growth inhibition was documented after transfection with p16(INK4a), p21(WAF1/Cip-1), and p53 in both SK-OV-3 cells and OVCA-420 cells. Apoptosis was greatest in SKOV-3 cells after transfection with p53. A significant expression of Bax was only seen in the SKOV-3 cells transfected with p53. The bcl-2 protein was poorly expressed in both cell lines. Expression of pRb was suppressed in OVCA-420 cells transfected with p16(INK4a) and p21(WAF1/Cip-1). Infection with Adp16(INK4a) and Adp53 led to an increase in the level of mdm-2 in the SK-OV-3 cell line only. CONCLUSIONS: In the ovarian cancer cell lines studied, cell growth was inhibited after transfection with p16(INK4a), p21(WAF1/Cip-1), and p53. Cell cycle arrest was highest with p53 transfection. The expression of pro-apoptosis proteins was primarily a function of p53 expression.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias Ováricas
/
Genes p53
/
Ciclinas
/
Inhibidor p16 de la Quinasa Dependiente de Ciclina
Límite:
Female
/
Humans
Idioma:
En
Revista:
Gynecol Oncol
Año:
2001
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Estados Unidos