Induction of apoptosis in human gastric cancer by sodium butyrate
Novel therapeutic agents are needed in the adjuvant treatment of gastric cancer. The differentiating agent sodium butyrate (NaBT) inhibits the growth of colon cancer cells; its effects on gastric cancers are not known. The purpose of our study was to characterize the effects of NaBT on human gastric...
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Published in: | Anticancer research Vol. 20; no. 2A; p. 779 |
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Abstract | Novel therapeutic agents are needed in the adjuvant treatment of gastric cancer. The differentiating agent sodium butyrate (NaBT) inhibits the growth of colon cancer cells; its effects on gastric cancers are not known. The purpose of our study was to characterize the effects of NaBT on human gastric cancer.
The human gastric cancer, SIIA, was treated with NaBT (5 mM) for 12-72 h. Cell number, viability and death were measured. Expression levels of the tumor-suppressor protein, p53, the cell-cycle inhibitors, p21Waf1/Cip1 and p27Kip1, and the pro-apoptotic proteins, Bax, Bak, and Bik, were determined.
NaBT significantly inhibited SIIA gastric cancer cell proliferation in a time-dependent fashion by a process involving the induction of apoptosis. Treatment with NaBT was associated with increased expression levels of p21Waf1/Cip1 p27Kip1, Bax, Bak, and Bik.
NaBT triggers growth arrest and apoptosis in the human gastric cancer SIIA potentially through the induction of the cell-cycle inhibitors, p21Waf1/Cip1 and p27Kip1, and the proapoptotic genes, Bax, Bak, and Bik. NaBT may be an effective adjuvant agent in the treatment of gastric cancer. |
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AbstractList | Novel therapeutic agents are needed in the adjuvant treatment of gastric cancer. The differentiating agent sodium butyrate (NaBT) inhibits the growth of colon cancer cells; its effects on gastric cancers are not known. The purpose of our study was to characterize the effects of NaBT on human gastric cancer.
The human gastric cancer, SIIA, was treated with NaBT (5 mM) for 12-72 h. Cell number, viability and death were measured. Expression levels of the tumor-suppressor protein, p53, the cell-cycle inhibitors, p21Waf1/Cip1 and p27Kip1, and the pro-apoptotic proteins, Bax, Bak, and Bik, were determined.
NaBT significantly inhibited SIIA gastric cancer cell proliferation in a time-dependent fashion by a process involving the induction of apoptosis. Treatment with NaBT was associated with increased expression levels of p21Waf1/Cip1 p27Kip1, Bax, Bak, and Bik.
NaBT triggers growth arrest and apoptosis in the human gastric cancer SIIA potentially through the induction of the cell-cycle inhibitors, p21Waf1/Cip1 and p27Kip1, and the proapoptotic genes, Bax, Bak, and Bik. NaBT may be an effective adjuvant agent in the treatment of gastric cancer. |
Author | Litvak, D A Evers, B M Hwang, K O Townsend, Jr, C M |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/10810354$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Apoptosis - drug effects Apoptosis Regulatory Proteins bcl-2 Homologous Antagonist-Killer Protein bcl-2-Associated X Protein Butyrates - toxicity Cell Cycle Proteins Cell Death - drug effects Cell Division - drug effects Cell Survival - drug effects Cyclin-Dependent Kinase Inhibitor p21 Cyclin-Dependent Kinase Inhibitor p27 Cyclins - genetics Gene Expression Regulation, Neoplastic - drug effects Genes, bcl-2 Genes, p53 Humans Membrane Proteins - genetics Microtubule-Associated Proteins - genetics Proteins - genetics Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-bcl-2 Stomach Neoplasms Tumor Cells, Cultured Tumor Suppressor Proteins |
Title | Induction of apoptosis in human gastric cancer by sodium butyrate |
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