2001PubMedRequires access

Apoptosis inducing effects of arsenic trioxide on human bladder cancer cell line BIU-87.

Qiang Tong, Fanchang Zeng, Liang-dong Zheng, Junjun Zhao, Lu Gao

Open publisher page 11 citations

Abstract

OBJECTIVE: To explore the apoptosis inducing effects of arsenic trioxide (As2O3) on human bladder cancer cells and elucidate possible mechanisms. METHODS: After treatment with As2O3, the growth inhibition rates of human bladder cancer cell line BIU-87 were studied by MTT and cell counts methods. DNA synthesis rates were detected by 3H-TdR assay. The morphological changes of cancer cells were observed by light and electronic microscopy and cell apoptosis rates were detected by TdT-mediated dUTP nick end labeling (TUNEL). bcl-2 gene expression of BIU-87 cells was observed by strept avidin-biotin complex (SABC) immunohistochemical method. RESULTS: As2O3 could effectively inhibit the growth of BIU-87 (P < 0.05), which were time and concentration dependent. The inhibition rate of 4.0 mumol/L As2O3 for DNA synthesis of cancer cells was 55.64% (P < 0.01). Partial cancer cells presented the characteristic morphological changes of apoptosis which depended on the time of exposure to drug (P < 0.05). bcl-2 expression of BIU-87 cells was decreased significantly (P < 0.05). CONCLUSION: As2O3 can significantly induce apoptosis in bladder cancer cells by down-regulating the expression of the bcl-2 gene and inhibiting DNA synthesis. This provides a potentially effective method for prevention and cure of human bladder cancer.

About this research paper

What this paper is about

OBJECTIVE: To explore the apoptosis inducing effects of arsenic trioxide (As2O3) on human bladder cancer cells and elucidate possible mechanisms. METHODS: After treatment with As2O3, the growth inhibition rates of human bladder cancer cell line BIU-87 were studied by MTT and cell counts methods. DNA synthesis rates were detected by 3H-TdR assay. The morphological changes of cancer cells were observed by light and electronic microscopy and cell apoptosis rates were detected by TdT-mediated dUTP nick end labeling (TUNEL). bcl-2 gene expression of BIU-87 cells was observed by strept avidin-biotin complex (SABC) immunohistochemical method. RESULTS: As2O3 could effectively inhibit the growth of BIU-87 (P < 0.05), which were time and concentration dependent. The inhibition rate of 4.0 mumol/L As2O3 for DNA synthesis of cancer cells was 55.64% (P < 0.01). Partial cancer cells presented the characteristic morphological changes of apoptosis which depended on the time of exposure to drug (P < 0.05). bcl-2 expression of BIU-87 cells was decreased significantly (P < 0.05). CONCLUSION: As2O3 can significantly induce apoptosis in bladder cancer cells by down-regulating the expression of the bcl-2 gene and inhibiting DNA synthesis. This provides a potentially effective method for prevention and cure of human bladder cancer.

Why it matters

OpenAlex reports 11 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

OBJECTIVE: To explore the apoptosis inducing effects of arsenic trioxide (As2O3) on human bladder cancer cells and elucidate possible mechanisms. METHODS: After treatment with As2O3, the growth inhibition rates of human bladder cancer cell line BIU-87 were studied by MTT and cell counts methods. DNA synthesis rates were detected by 3H-TdR assay. The morphological changes of cancer cells were observed by light and electronic microscopy and cell apoptosis rates were detected by TdT-mediated dUTP nick end labeling (TUNEL). bcl-2 gene expression of BIU-87 cells was observed by strept avidin-biotin complex (SABC) immunohistochemical method. RESULTS: As2O3 could effectively inhibit the growth of BIU-87 (P < 0.05), which were time and concentration dependent. The inhibition rate of 4.0 mumol/L As2O3 for DNA synthesis of cancer cells was 55.64% (P < 0.01). Partial cancer cells presented the characteristic morphological changes of apoptosis which depended on the time of exposure to drug (P < 0.05). bcl-2 expression of BIU-87 cells was decreased significantly (P < 0.05). CONCLUSION: As2O3 can significantly induce apoptosis in bladder cancer cells by down-regulating the expression of the bcl-2 gene and inhibiting DNA synthesis. This provides a potentially effective method for prevention and cure of human bladder cancer.

Key concepts: Arsenic trioxide, Apoptosis, TUNEL assay, Bladder cancer, Cancer cell, Cancer research, Molecular biology, Cell culture

Related papers

Back to paper searchBrowse research topicsOriginal source
Apoptosis inducing effects of arsenic trioxide on human bladder cancer cell line BIU-87. — Research Paper | ScholarLens