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1.
Chinese Journal of General Surgery ; (12)2001.
Artículo en Chino | WPRIM | ID: wpr-521156

RESUMEN

Objective To study the effect of Fas gene transfection on rectal carcinoma cells in vitro. Methods By using RT-PCR technique, a full length of Fas gene 1007 bp was cloned from actived peripheral mononuclear cells of healthy donors. The fragment was ligated with the pGEM-T Easy and sequenced. The constructed vector was transfected into 8348 cells with lipofectin, the change in expression of Fas gene was determined by RT-PCR. The apoptosis and proliferation of rectal carcinoma cells pre- and posttransfection induced by cisplatin were analysed by ladder and MTT methods. Results Transfection of Fas gene significantly upregulates the expression of Fas in human rectal carcinoma 8348 cells. With the concentration of cisplatin at the level of 1, 5, 10, 20 and 40 mg/L , respectively, the suppression rates of Fas transfection group and control group were 47.2%51.8%57.2%65.4%71.0% and 29.6%33.0%37.8%41.4%47.0% respectively(t=15.33, P

2.
Medical Journal of Chinese People's Liberation Army ; (12)2001.
Artículo en Chino | WPRIM | ID: wpr-552333

RESUMEN

To evaluate the inhibitory effects of fas gene transduction on oesophageal cancer cells in vitro, the eukaryotic expression vector fas pBK was constructed and transfected into oesophageal carcinoma cells EC109. Western blot results showed high expression of Fas protein in gene transfected cells Fas EC109. Cell growth curve and plating efficiency test revealed that Fas EC109 had longer population doubling time and lower plating efficiency compared with control cells. Results of MTT assay showed increased sensitivity of Fas EC109 cells to CDDP, VCR and 5 FU. All these data suggested that transgenic expression of fas gene could effectively inhibit the proliferation and increase the drug sensitivity of oesophageal carcinoma cells in vitro.

3.
Chinese Journal of General Surgery ; (12)1993.
Artículo en Chino | WPRIM | ID: wpr-517575

RESUMEN

Objective To investigate the influence of ?-interferon (?-IFN) on liver cancer cell line (Hep-G2). Methods Observing the expression of Fas and Bcl-2 by ?-IFN-pretreated Hep-G2 cells via immunohistochemical stain; subsequently treating these cells with adrimysin, and observing the cell death rate and apoptosis of these cell by MTT and electroscopy. Results (1) ?-IFN up-regulating the expression of Fas protein and down-regulating Bcl-2 protein (P

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