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[重组RA538及反义C-myc腺病毒对高表达Bcl-2基因的人胃癌、食管癌细胞系生物学效应及分子机制的体内外研究]

[In vitro and in vivo studies on the biologic effects and molecular mechanism of recombinant RA538 and antisense C-myc adenovirus on human gastric, esophageal and cancer cell lines with high-expression of Bcl-2 gene].

作者信息

Chen J P

机构信息

Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038.

出版信息

Sheng Li Ke Xue Jin Zhan. 1999 Jul;30(3):227-30.

Abstract

In this study, the biological effects and molecular mechanism of recombinant RA538 and antisense c-myc adenovirus on human gastric, esophageal, 2BS and high-expression bcl-2 gene cancer cell lines were studied in vitro and in vivo. The results were as follows: Ad-RA538 and Ad-ASc-myc could strongly inhibit cell growth and induce apoptosis of SGC7901 cells in vitro and in vivo, and could down-regulate expression of c-myc, bcl-2 and cyclinD1 gene, up-regulate expression of bax gene. Ad-RA538 or Ad-AS c-myc could not inhibit cell growth and induce apoptosis changes of EC109, EC8712, 2BS and high-expression bcl-2 gene cancer cell lines, and could not down-regulate expression of c-myc and bcl-2 gene. The results indicated that: Ad-RA538 or Ad-AS c-myc can inhibit growth and induce apoptosis of gastric cancer cell in vitro and in vivo. They relate to c-myc, bcl-2, cyclinD1 and bax gene closely and play a key role on biologic effects in gastric cancer cells. Ad-RA538 and Ad-AS c-myc could not produce relevant changes on esophageal cancer, 2BS and high-expression bcl-2 gene cell lines.

摘要

本研究在体内外研究了重组RA538和反义c-myc腺病毒对人胃癌、食管癌、2BS细胞及高表达bcl-2基因癌细胞系的生物学效应及分子机制。结果如下:Ad-RA538和Ad-ASc-myc在体内外均能强烈抑制SGC7901细胞生长并诱导其凋亡,且能下调c-myc、bcl-2和cyclinD1基因表达,上调bax基因表达。Ad-RA538或Ad-AS c-myc对EC109、EC8712、2BS及高表达bcl-2基因癌细胞系无抑制细胞生长及诱导凋亡的作用,也不能下调c-myc和bcl-2基因表达。结果表明:Ad-RA538或Ad-AS c-myc在体内外均可抑制胃癌细胞生长并诱导其凋亡。它们与c-myc、bcl-2、cyclinD1和bax基因密切相关,对胃癌细胞的生物学效应起关键作用。Ad-RA538和Ad-AS c-myc对食管癌细胞、2BS细胞及高表达bcl-2基因细胞系无相关作用。

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