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| Effects of arsenic trioxide on human renal cell carcinoma lines in vitro |
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| KeyWord:renal cell carcinoma arsenic trioxide apoptosis cell cycle arrest |
| Author Name | Affiliation | | Qu Feng-lian | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing | | Li Yan-fen | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing | | Wan Yun-xia | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing | | Ma Jian-hui | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing | | Shi Wei | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing | | Chu Da-tong | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing | | Sun Yan | Coordinating Group of Biologic Therapy, Cancer Hospital, Chinese Academy of Medical Sciences, 100021, Beijing |
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| 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-proliferative 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, p53and 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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