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Chinese Journal of Pancreatology ; (6): 84-87, 2008.
Artigo em Chinês | WPRIM | ID: wpr-401620

RESUMO

Objective To investigate the inhibitory effect of proliferation and invasiveness on PANC1 cell by knockdown of NF-κB P65 expression through RNA interference. Methods Chemically synthesized small interference RNA (siRNA) directed against human NF-κB p65 was transfected into pancreatic carcinoma cell (PANC1) by using cationic liposome LipofectamineTM 2000 as the transfection agent. A non-silencing siRNA was used as the negative control and distilled water was used as the blank control. The tests repeated for six times. The expression of NF-KB p65 and ICAM-1 gone was detected by RT-PCR. The effect of cell proliferation and invasive ability was evaluated by MTF, clony assay, Matrigel invasive tests. Results The relative expression levels of NF-κB p65 mRNA in siRNA, the negative control and the blank control group were 0.227 ±0.045, O. 381 ± 0. 038 and 0. 404 ± 0. 031, respectively; the relative expression levels of ICAM-1mRNA were 0.597 ± 0. 083, 0.983 ± 0.068 and 1. 027 ± 0.098, respectively; the inhibitory rate of the cells at 72h were 18.3%, 2.3% and 0, respectively; the colony forming efficiency were ( 14.1 ± 3.1 ) %, ( 24.5±2.1)% and (27.2 ±2.6)%, respectively; the number of invasive cells were 80.25 ±6.35, 123.83 ±8.80 and 127.68 ± 9.23, respectively; the difference between the siRNA group and two control groups was significant (P < 0. 01 ). Conclusions Down-regulatiag the expression of NF-κB p65 gene by RNAi may inhibit proliferation and invasiveness in pancreatic carcinoma cell strain PANC1.

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