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Acta Academiae Medicinae Sinicae ; (6): 155-163, 2016.
Article Dans Chinois | WPRIM | ID: wpr-289888

Résumé

<p><b>OBJECTIVE</b>To investigate the effect and regulatory mechanism of clock gene Per1 on the proliferation,apoptosis,migration,and invasion of human oral squamous carcinoma SCC15 cells.</p><p><b>METHODS</b>RNA interference was used to knock down Per1 gene in human oral squamous cell carcinoma SCC15 cell line. Changes of cell proliferation and apoptosis were analyzed by flow cytometry. Transwell assay was carried out to assess cell migration and invasion. Real-time polymerase chain reaction was used to detect the mRNA expressions of Ki-67, murine double minute 2 (MDM2), c-Myc, p53, Bax, Bcl-2, metalloproteinase (MMP)2, MMP9, and vascular endothelial growth factor (VEGF).</p><p><b>RESULTS</b>shRNA-mediated knockdown of Per1 promoted the proliferation, migration and invasion capacity, and inhibited cell apoptosis capacity of SCC15 cells (all P<0.05). Additionally, Per1 knockdown also increased the mRNA expressions of Ki-67, MDM2, Bcl-2, MMP2, and MMP9 and decreased the mRNA expressions of c-Myc, p53, and Bax (all P<0.05); however, the VEGF mRNA expression did not differ significantly after Per1 knockdown (P>0.05).</p><p><b>CONCLUSIONS</b>Clock gene Perl can regulate important tumor-related genes downstream such as Ki-67, MDM2, c-Myc, p53, Bax, Bcl-2, MMP2, and MMP9, and the aberrant expression of Per1 can affect tumor cell proliferation,apoptosis,migration and invasion. An in-depth study of Per1 may further clarify the mechanism of tumorigenesis and tumor development and thus provides new effective molecular targets for cancer treatment.</p>


Sujets)
Humains , Apoptose , Carcinome épidermoïde , Métabolisme , Lignée cellulaire tumorale , Mouvement cellulaire , Prolifération cellulaire , Techniques de knock-down de gènes , Antigène KI-67 , Métabolisme , Matrix metalloproteinase 2 , Métabolisme , Matrix metalloproteinase 9 , Métabolisme , Protéines circadiennes Period , Métabolisme , Protéines proto-oncogènes c-bcl-2 , Métabolisme , Protéines proto-oncogènes c-mdm2 , Métabolisme , Protéines proto-oncogènes c-myc , Métabolisme , Interférence par ARN , Réaction de polymérisation en chaine en temps réel , Protéine p53 suppresseur de tumeur , Métabolisme , Facteur de croissance endothéliale vasculaire de type A , Métabolisme , Protéine Bax , Métabolisme
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