Abstract
The effect of B cell-specific MLV integration site-1 (Bmi-1) RNA interference (RNAi)-mediated inhibition of Bmi-1 expression on the proliferation, apoptosis, and invasiveness of human gastric carcinoma AGS cells was investigated. RT-PCR and Western blot analyses demonstrated that Bmi-1 expression and the Bmi-1 protein level were significantly decreased in Bmi-1 shRNA transfected AGS cells compared to untransfected and nonspecific shRNA transfected AGS cells. Bmi-1 RNAi-mediated inhibition of Bmi-1 expression significantly affected cell growth and invasiveness, and resulted in increased AGS cell apoptosis. This was not observed in untransfected and nonspecific shRNA transfected AGS cells. Inhibition of Bmi-1 expression in human gastric carcinoma cells affects cell proliferation and invasiveness.
MeSH terms
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Cell Line, Tumor
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Cell Proliferation
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Cyclin-Dependent Kinase Inhibitor p16 / physiology
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Humans
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Neoplasm Invasiveness
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Nuclear Proteins / antagonists & inhibitors*
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Nuclear Proteins / genetics
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Nuclear Proteins / physiology
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Polycomb Repressive Complex 1
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Proto-Oncogene Proteins / antagonists & inhibitors*
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / physiology
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RNA Interference
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RNA, Small Interfering / genetics
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Repressor Proteins / antagonists & inhibitors*
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Repressor Proteins / genetics
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Repressor Proteins / physiology
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Stomach Neoplasms / pathology*
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Tumor Suppressor Protein p14ARF / physiology
Substances
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BMI1 protein, human
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Cyclin-Dependent Kinase Inhibitor p16
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Nuclear Proteins
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Proto-Oncogene Proteins
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RNA, Small Interfering
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Repressor Proteins
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Tumor Suppressor Protein p14ARF
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Polycomb Repressive Complex 1