Arsenic trioxide inhibiting the proliferation and inducing apoptosis of human renal cell carcinoma 786-0 cells in vitro
Delin Wang
Abstract
Delin Wang
Abstract
Objective To explore the anti-proliferative effects of arsenic trioxide on human renal cell carcinoma 786-0 cells and its mechanisms.Methods The anti-tumor effects of arsenic trioxide were analyzed by the cell proliferation,cell morphology,DNA gel electrophoresis and tumor colony formation,and the mechanism was studied by immunocytochemistry and RT-PCR.Results After 786-0 cells were treated with arsenic trioxide of more than 2 μmol/L for 72 h,arsenic trioxide could effectively inhibit 69.13% of the proliferation of 786-0 cells (P 0.01), and the karyokinesis index of 786-0 cells was also decreased significantly (P 0.01). Arsenic trioxide prohibited nearly 100.00% of tumor colony formation of 786-0 cells (P 0.01). It significantly down-regulated the expression of bcl-2 and PCNA and Ki-67 genes in 786-0 cells (P 0.01), and induced the apoptotic morphology and DNA fragmentation of 786-0 cells in a time- and concentration-dependent manner.Conclusion Arsenic trioxide can inhibit the growth of 786-0 significantly in a dose- and time-dependent manner possibly by the down-regulation of PCNA and Ki-67 genes caused by arsenic trioxide.Induced apoptosis by arsenic trioxide appears to be associated with down-regulation of the expression of bcl-2 gene.
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Objective To explore the anti-proliferative effects of arsenic trioxide on human renal cell carcinoma 786-0 cells and its mechanisms.Methods The anti-tumor effects of arsenic trioxide were analyzed by the cell proliferation,cell morphology,DNA gel electrophoresis and tumor colony formation,and the mechanism was studied by immunocytochemistry and RT-PCR.Results After 786-0 cells were treated with arsenic trioxide of more than 2 μmol/L for 72 h,arsenic trioxide could effectively inhibit 69.13% of the proliferation of 786-0 cells (P 0.01), and the karyokinesis index of 786-0 cells was also decreased significantly (P 0.01). Arsenic trioxide prohibited nearly 100.00% of tumor colony formation of 786-0 cells (P 0.01). It significantly down-regulated the expression of bcl-2 and PCNA and Ki-67 genes in 786-0 cells (P 0.01), and induced the apoptotic morphology and DNA fragmentation of 786-0 cells in a time- and concentration-dependent manner.Conclusion Arsenic trioxide can inhibit the growth of 786-0 significantly in a dose- and time-dependent manner possibly by the down-regulation of PCNA and Ki-67 genes caused by arsenic trioxide.Induced apoptosis by arsenic trioxide appears to be associated with down-regulation of the expression of bcl-2 gene.
Key concepts: Arsenic trioxide, Apoptosis, Cell growth, Chemistry, Arsenic, Proliferating cell nuclear antigen, In vitro, Molecular biology