Role of short haipin RNA targeting vascular endothelial growth factor-C on biological characteristics of human breast cancer cell MCF-7 / 中华病理学杂志
Chinese Journal of Pathology
;
(12): 472-476, 2009.
Article
Dans Chinois
| WPRIM
| ID: wpr-249127
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of short haipin RNA (shRNA) on expression of vascular endothelial growth factor C (VEGF-C) and proliferation and invasion behavior of human breast cancer cell MCF-7.</p><p><b>METHODS</b>The recombinant vector (pSIREN-VEGF-C) was transfected into the human breast cancer cell MCF-7 by liposome and the positive transfected cell clones were screened with puromycin. Expression of VEGF-C in MCF-7 cells after gene transfer was detected by real-time quantitative PCR and Western blot assay, respectively. Proliferation and invasion ability of transfected cells were analyzed by MTT and Transwell filter.</p><p><b>RESULTS</b>The expressions of VEGF-C mRNA and protein were decreased markedly compared with the control group after the transfection and the inhibitive ratio was 95% and 100% respectively (P<0.05). The proliferation of MCF-7 cells transfected by pSIREN-VEGF-C, measured with MTT assays, was significantly decended (P<0.05). The invasion ability of passing through the Transwell filter of MCF-7 cells transfected by pSIREN-VEGF-C were declined evidently (P<0.05).</p><p><b>CONCLUSION</b>The recombinant vector (pSIREN-VEGF-C) have been proved not only to be effective and specific for down-regulation of VEGF-C, but also can inhibit the proliferation and invasion of MCF-7 cells significantly.</p>
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Anatomopathologie
/
Protéines recombinantes
/
Tumeurs du sein
/
ARN messager
/
Transfection
/
Régulation négative
/
Petit ARN interférent
/
Interférence par ARN
/
Lignée cellulaire tumorale
/
Facteur de croissance endothéliale vasculaire de type C
Limites du sujet:
Femelle
/
Humains
langue:
Chinois
Texte intégral:
Chinese Journal of Pathology
Année:
2009
Type:
Article
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