Yong-En Xie1, En-Jie Tang, Da-Rong Zhang, Bi-Xuan Ren. 1. The Institute of Immunology and Molecular Biology, North Sichuan Medical College, No.234, Fujiang Road, Nanchong 637007, Sichuan Province, China. xyongen@sina.com
Abstract
AIM: To determine the inhibitory effect of the vector-generated small interfering RNAs (siRNAs) on the expression of the Bcl-X(L) gene in established human esophageal cancer cells, and to investigate the effect of the Bcl-X(L) siRNAs on cell growth and apoptosis in esophageal cancer cells. METHODS: Three siRNA-expressing vectors targeting different sites of the Bcl-X(L) gene were constructed from pTZ-U6+1 vector. Cultured esophageal cancer cells were transfected with the siRNA-expressing vector (or the control vector) using lipofectamine 2000. Bcl-X(L) gene expression was determined with semiquantitative RT-PCR assay and Western blotting. Among the three siRNA-expressing vectors, the most highly functional vector and its effect on cell growth and apoptosis in esophageal cancer cells was further analyzed. RESULTS: Of the three siRNA-expressing vectors, siRNA-expressing vector No.1 was the most potent one which suppressed Bcl-X(L) mRNA production to 32.5% of that in the untreated esophageal cancer cells. Western blotting analysis showed that siRNA-expressing vector No.1 markedly down-regulated the expression of Bcl-X(L) in human esophageal cancer cells. Treatment of esophageal cancer cells with siRNA-expressing vector No.1 resulted in inhibition of cell growth and induction of apoptosis. CONCLUSION: Down-regulation of Bcl-X(L) by vector-generated small interfering RNAs can suppress cell growth and induce apoptosis in human esophageal cancer cells.
AIM: To determine the inhibitory effect of the vector-generated small interfering RNAs (siRNAs) on the expression of the Bcl-X(L) gene in established humanesophageal cancer cells, and to investigate the effect of the Bcl-X(L) siRNAs on cell growth and apoptosis in esophageal cancer cells. METHODS: Three siRNA-expressing vectors targeting different sites of the Bcl-X(L) gene were constructed from pTZ-U6+1 vector. Cultured esophageal cancer cells were transfected with the siRNA-expressing vector (or the control vector) using lipofectamine 2000. Bcl-X(L) gene expression was determined with semiquantitative RT-PCR assay and Western blotting. Among the three siRNA-expressing vectors, the most highly functional vector and its effect on cell growth and apoptosis in esophageal cancer cells was further analyzed. RESULTS: Of the three siRNA-expressing vectors, siRNA-expressing vector No.1 was the most potent one which suppressed Bcl-X(L) mRNA production to 32.5% of that in the untreated esophageal cancer cells. Western blotting analysis showed that siRNA-expressing vector No.1 markedly down-regulated the expression of Bcl-X(L) in humanesophageal cancer cells. Treatment of esophageal cancer cells with siRNA-expressing vector No.1 resulted in inhibition of cell growth and induction of apoptosis. CONCLUSION: Down-regulation of Bcl-X(L) by vector-generated small interfering RNAs can suppress cell growth and induce apoptosis in humanesophageal cancer cells.
Authors: Y Tu; S Renner; F Xu; A Fleishman; J Taylor; J Weisz; R Vescio; M Rettig; J Berenson; S Krajewski; J C Reed; A Lichtenstein Journal: Cancer Res Date: 1998-01-15 Impact factor: 12.701
Authors: S Kondo; Y Shinomura; S Kanayama; Y Higashimoto; J I Miyagawa; T Minami; T Kiyohara; S Zushi; S Kitamura; K Isozaki; Y Matsuzawa Journal: Int J Cancer Date: 1996-12-11 Impact factor: 7.396
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