Effect of shRNA-mediated silence of H-ras gene on proliferation of human SACC-M cells / 中华口腔医学杂志
Chinese Journal of Stomatology
;
(12): 113-117, 2008.
Artículo
en Chino
| WPRIM
| ID: wpr-235971
ABSTRACT
<p><b>OBJECTIVE</b>To examine the effects of H-ras gene silence on cell cycle, proliferation and apoptosis of salivary adenoid cystic carcinoma -M (SACC-M) cell lines.</p><p><b>METHODS</b>The plasmid H-ras-shRNA, containing the sequence of shRNA targeting H-ras, and HK-shRNA (without interfering effect) were constructed and transfected into SACC-M cells. The cell line with shRNA plasmid stable expression was isolated by G418. The expression levels of H-ras were detected by RT-PCR and protein immunofluorescent assay; cell cycle and cell apoptosis were analyzed by flow cytometry (FCM). The proliferation of cell was also determined by subcutaneous tumor formation in nude mice.</p><p><b>RESULTS</b>After transfection of H-ras-shRNA plasmid, the mRNA expression of H-ras in SACC-M cells was down-regulated by 61.80% and protein expression of H-ras was inhibited by 62.76%; the cell proliferation was inhibited obviously; the G0G1 phase cells were increased. The cell apoptosis rate of H-ras-shRNA group was significantly higher than that of HK-shRNA group (P <0.05). The volume of subcutaneous tumor in nude mice was significantly smaller in Hras-shRNA group than in control group.</p><p><b>CONCLUSIONS</b>The recombinant plasmid HRAS-shRNA could efficiently down-regulate the expression of H-ras gene and protein, induce apoptosis of SACC-M cells and simultaneously inhibit proliferation of these cells in vitro and in vivo.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Patología
/
Neoplasias de las Glándulas Salivales
/
Transfección
/
Proteínas Proto-Oncogénicas p21(ras)
/
Apoptosis
/
Carcinoma Adenoide Quístico
/
Silenciador del Gen
/
ARN Interferente Pequeño
/
Línea Celular Tumoral
/
Proliferación Celular
Límite:
Animales
/
Femenino
/
Humanos
Idioma:
Chino
Revista:
Chinese Journal of Stomatology
Año:
2008
Tipo del documento:
Artículo
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