Ai zheng = Aizheng = Chinese journal of cancer · 2008
[Inhibitory effect of adriamycin combined P21CIP1 gene transfection on proliferation of human hepatoblastoma cell line HepG2].
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Xiong Juan, Hu Li-Hua, Li Yi-Rong, Wang Lin
Аннотация
BACKGROUND & OBJECTIVE: Chemotherapy protocols using adriamycin (ADM) is a standard treatment for hepatoblastoma, but the treatment results became unsatisfied because of drug resistance. Recently, ADM combined gene therapy is a developing alternative treatment for hepatoblastoma. This study was to investigate the effect of ADM combined human p21CIP1 transfection on the proliferation of hepatoblastoma cell line HepG2.
METHODS: HepG2 cells were divided into empty control group (no treatment), ADM group (treated with 0.5 microg/mL ADM), blank control group (transfected with blank plasmid pcDNA3), p21 group (transfected with plasmid pcDNA3-p21), and combination group (ADM treatment plus p21 transfection). The proliferation of HepG2 cells was observed by MTT assay. The mRNA levels of p21 and survivin were detected by real-time polymerase chain reaction (PCR).
RESULTS: After transfection, the mRNA level of p21 in p21 group was increased by 155 folds of that in empty control group (P<0.05). p21 inhibited the proliferation of HepG2 cells at Day 3 and Day 4 after transfection (P<0.01). The proliferation inhibition rate was significantly higher in combination group than in ADM group and p21 group (43.92% vs. 32.97% and 35.77% at Day 3, P<0.01; 59.86% vs. 39.35% and 40.96% at Day 4, P<0.01; 51.81% vs. 33.91% and 10.68% at Day 5, P<0.01). This effect was enhanced along with the increasing time of co-treatment from Day 1 to Day 4 (r=0.91, P<0.05), and it was obvious at Day 4 (Q =1.07). The mRNA level of survivin was significantly lower in combination group than in p21 group and ADM group (P<0.01).
CONCLUSION: p21 gene transfection plus ADM can inhibit the proliferation of HepG2 cells and down-regulate the level of survivin mRNA, thus may be a potential therapeutic strategy against human hepatoblastoma.
METHODS: HepG2 cells were divided into empty control group (no treatment), ADM group (treated with 0.5 microg/mL ADM), blank control group (transfected with blank plasmid pcDNA3), p21 group (transfected with plasmid pcDNA3-p21), and combination group (ADM treatment plus p21 transfection). The proliferation of HepG2 cells was observed by MTT assay. The mRNA levels of p21 and survivin were detected by real-time polymerase chain reaction (PCR).
RESULTS: After transfection, the mRNA level of p21 in p21 group was increased by 155 folds of that in empty control group (P<0.05). p21 inhibited the proliferation of HepG2 cells at Day 3 and Day 4 after transfection (P<0.01). The proliferation inhibition rate was significantly higher in combination group than in ADM group and p21 group (43.92% vs. 32.97% and 35.77% at Day 3, P<0.01; 59.86% vs. 39.35% and 40.96% at Day 4, P<0.01; 51.81% vs. 33.91% and 10.68% at Day 5, P<0.01). This effect was enhanced along with the increasing time of co-treatment from Day 1 to Day 4 (r=0.91, P<0.05), and it was obvious at Day 4 (Q =1.07). The mRNA level of survivin was significantly lower in combination group than in p21 group and ADM group (P<0.01).
CONCLUSION: p21 gene transfection plus ADM can inhibit the proliferation of HepG2 cells and down-regulate the level of survivin mRNA, thus may be a potential therapeutic strategy against human hepatoblastoma.