Feng-lian, Q., Yan-fen, L., Yun-xia, W. et al. Effects of arsenic trioxide on human renal cell carcinoma lines in vitro., Chin. J. Integr. Med. 10, 48–51 (2004). https://doi.org/10.1007/BF02836561
Qu Feng-lian, Li Yan-fen, Wan Yun-xia, et al. Effects of arsenic trioxide on human renal cell carcinoma lines in vitro. [J]. Chinese Journal of Integrative Medicine 10(1):48-51(2004)
Feng-lian, Q., Yan-fen, L., Yun-xia, W. et al. Effects of arsenic trioxide on human renal cell carcinoma lines in vitro., Chin. J. Integr. Med. 10, 48–51 (2004). https://doi.org/10.1007/BF02836561DOI:
Qu Feng-lian, Li Yan-fen, Wan Yun-xia, et al. Effects of arsenic trioxide on human renal cell carcinoma lines in vitro. [J]. Chinese Journal of Integrative Medicine 10(1):48-51(2004) DOI: 10.1007/BF02836561.
Effects of arsenic trioxide on human renal cell carcinoma lines in vitro
摘要
Objective: To observe the effects of arsenic trioxide (As2O3) on human renal cell carcinoma (RCC) lines in vitro and to explore its possible molecular mechanisms.Methods: The microculture tetrazolium (MTT) assay was used to determine the anti-proliterative effects of As2O3 on human RCC lines. Flow cytometry was performed to investigate the effects of As2O3 on cell cycle and cell apoptosis. The reverse transcription-polymerase chain reaction (RT-PCR) was conducted to detect mRNA expression of Bcl-2
Bax
p53 and c-myc.Results: As2O3 inhibited the growth of RCC lines in vitro in a concentration-dependent manner. At the concentrations of 0.5
1.0
2.0 and 4. 0 μmol/L
the inhibition rates of As2O3 on RCC-WCS cells were 27.60%
30.09%
41.03% and 50.77%
respectively. Compared with untreated RCC-WCS
there was significant difference at each concentration (P<0.01). As2O3 induced a G1 phase arrest in RCC-LSL cells
but a G2/M phase arrest in RCC-WCS and RCC-SHK. As2O3 induced cell apoptosis in these cell lines. The mRNA level of p53 and c-myc decreased
but no detectable changes of Bcl-2 and Bax were observed after As2O3 treatmen.Conclusion: As2O3 in therapeutic concentrations inhibited the in vitro growth of RCC lines via cell cycle arrest and apoptosis. One of its possible mechanisms was down-regulation of p53 and c-myc. Our results suggest that As2O3 is probably a new candidate agent for the treatment of human renal carcinoma.
Abstract
Objective: To observe the effects of arsenic trioxide (As2O3) on human renal cell carcinoma (RCC) lines in vitro and to explore its possible molecular mechanisms.Methods: The microculture tetrazolium (MTT) assay was used to determine the anti-proliterative effects of As2O3 on human RCC lines. Flow cytometry was performed to investigate the effects of As2O3 on cell cycle and cell apoptosis. The reverse transcription-polymerase chain reaction (RT-PCR) was conducted to detect mRNA expression of Bcl-2
Bax
p53 and c-myc.Results: As2O3 inhibited the growth of RCC lines in vitro in a concentration-dependent manner. At the concentrations of 0.5
1.0
2.0 and 4. 0 μmol/L
the inhibition rates of As2O3 on RCC-WCS cells were 27.60%
30.09%
41.03% and 50.77%
respectively. Compared with untreated RCC-WCS
there was significant difference at each concentration (P<0.01). As2O3 induced a G1 phase arrest in RCC-LSL cells
but a G2/M phase arrest in RCC-WCS and RCC-SHK. As2O3 induced cell apoptosis in these cell lines. The mRNA level of p53 and c-myc decreased
but no detectable changes of Bcl-2 and Bax were observed after As2O3 treatmen.Conclusion: As2O3 in therapeutic concentrations inhibited the in vitro growth of RCC lines via cell cycle arrest and apoptosis. One of its possible mechanisms was down-regulation of p53 and c-myc. Our results suggest that As2O3 is probably a new candidate agent for the treatment of human renal carcinoma.
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