野生型P53、P16基因联合抑制人胃癌细胞HGC27生长的实验研究

doi:10.3969/j.issn.1004-616x.2004.06.008

Carcinogenesis, Teratogenesis & Mutagenesis ›› 2004, Vol. 16 ›› Issue (6): 344-346.doi: 10.3969/j.issn.1004-616x.2004.06.008

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Study on the Growth Inhibition of Human Gastric Carcinoma Cell HGC27 by Combination of Wild-Type P53, P16 Genes

ZHANG Hong-yu， SUN Qiang, WANG Ya-dong, et al

Shenzhen Center for Disease Prevention and Control,Shenzhen 518020,China

Received:2004-06-13 Revised:2004-09-25 Online:2004-11-30 Published:2004-11-30
Contact: ZHANG Hong-yu

Abstract

Abstract: BACKGROUND ＆ AIM: To investigate the suppression effect on human gastric carcinoma cell HGC27 by combination of wild-type P53, P16 genes mediated by retrovirus vector. METERIAL AND METHODS:Human gastric carcinoma cell line HGC27 was transfected via two retrovirus vectors pLNCX containing wild-type P53, P16 genes by lipofectamine. By using cell growth curve, MTT growth inhibition rate, Southern blot and flow cytometry assay, the clones obtained were detected and observed for the changes of their biologic characteristics. RESULTS:Overexpression of wild-type P53 and P16 gene inhibited the growth of human gastric carcinoma cell line. The HGC27 cell growth inhibition and apoptosis caused by combination transfection of wild-type P53 and P16 gene were higher than those caused by single gene transfection. CONCLUSION: The therapeutic effect of P53 and P16 gene combination therapy is significantly higher than that of single gene therapy.

Key words: gastric neoplasm, P53, P16, gene therapy

ZHANG Hong-yu, SUN Qiang, WANG Ya-dong, et al. Study on the Growth Inhibition of Human Gastric Carcinoma Cell HGC27 by Combination of Wild-Type P53, P16 Genes[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2004, 16(6): 344-346.

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Study on the Growth Inhibition of Human Gastric Carcinoma Cell HGC27 by Combination of Wild-Type P53, P16 Genes

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