Arsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitro

Akao, Yukihiro; Nakagawa, Yoshihito; Akiyama, Kiyotaka

doi:10.1016/s0014-5793(99)00841-8

Cited by 165 publications

(105 citation statements)

References 16 publications

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“…in human gastric cancer mGc-803 cells, as 2 O 3 was also found to inhibit cell growth and to induce cell apoptosis (7). Similar findings were observed in esophageal carcinoma (8), neuroblastoma (9), prostate and ovarian carcinoma (10), and breast cancer (11,12) cells. however, the molecular mechanisms underlying the as 2 O 3 -promoted apoptosis of solid tumor cells remain unknown.…”

Section: Introductionsupporting

confidence: 61%

Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels

Wang¹,

Zhang²,

Yang³

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. arsenic trioxide (as 2 O 3 ) has been widely used to treat patients with acute promyelocytic leukemia and has also been shown to exhibit therapeutic effects on various types of solid tumors, including gastric cancer and lung carcinoma. Breast cancer is a type of solid tumor whose incidence has been increasing for many years. the present study was designed to investigate the effects of as 2 O 3 on the human breast cancer cell line mcF-7, and to explore its potential mechanisms. the mtt assay demonstrated that as 2 O 3 decreased the cellular viability of mcF-7 cells in a concentration-dependent manner. morphological observation, the tunEl assay and flow cytometric analysis revealed that apoptosis was involved in the process. an assay for caspase-3 activity suggested that the apoptosis was mediated through caspase-3 activation. Further investigation indicated that protein levels of the human ether-a-go-go-related gene (hErG) were markedly downregulated by as 2 O 3 . taken together, the results indicate that arsenic trioxide induces the apoptosis of human breast cancer mcF-7 cells at least in part through the activation of caspase-3 and the decrease in hErG expression.

show abstract

Section: Introductionsupporting

confidence: 61%

Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels

Wang¹,

Zhang²,

Yang³

et al. 2011

Experimental and Therapeutic Medicine

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show abstract

“…In MGC-803 human gastric cancer cells, As 2 O 3 was shown to inhibit cell growth and to induce cell apoptosis (4). Similar findings were observed in esophageal carcinoma (5), neuroblastoma (6), prostate and ovarian carcinoma (7), and breast cancer (8) cells. Several mechanism of action involved in the As 2 O 3 -induced apoptosis of cancer cells have been identified (8,9).…”

Section: Introductionsupporting

confidence: 58%

Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells

Wang

Yin

et al. 2012

Molecular Medicine Reports

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Abstract. Arsenic trioxide (As 2 O 3 ) has been widely used in the treatment of acute promyelocytic leukemia and has been observed to exhibit therapeutic effects in various types of solid tumor. In a previous study by this group, it was shown that As 2 O 3 induces the apoptosis of MCF-7 breast cancer cells through inhibition of the human ether-à-go-go-related gene (hERG) channel. The present study was designed to further investigate the effect of As 2 O 3 on breast cancer cells and to examine the mechanism underlying the regulation of hERG expression. The present study confirmed that As 2 O 3 inhibited tumor growth in vivo, following MCF-7 cell implantation into nude mice. Using computational prediction , it was identified that microRNA (miR)-328 had a binding site in the 3'-untranslated region of hERG mRNA. A luciferase activity assay demonstrated that hERG is a target gene of miR-328. Further investigation using western blot analysis and reverse transcription-quantitative polymerase chain reaction revealed that As 2 O 3 downregulated hERG expression via upregulation of miR-328 expression in MCF-7 cells. In conclusion, As 2 O 3 was observed to inhibit breast cancer cell growth, at least in part, through the miR-328/hERG pathway.

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“…However, subsequent investigations have demonstrated that As 2 O 3 broadly affects signal transduction pathways and causes many alterations in cellular functions leading to apoptosis (Miller, 2002;Miller et al, 2002). Recent studies demonstrate that not only hematological cancers other than APL but solid tumors derived from several tissues are susceptible to As 2 O 3 (Akao et al, 1999;Zhu et al, 1999;Kitamura et al, 2000;Grad et al, 2001;Ishitsuka et al, 2002;Maeda et al, 2002). However, the mechanisms underlying the antitumor effect of As 2 O 3 on solid tumors have yet to be clarified.…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide induces autophagic cell death in malignant glioma cells by upregulation of mitochondrial cell death protein BNIP3

et al. 2004

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Arsenic trioxide (As 2 O 3 ) has shown considerable efficacy in treating hematological malignancies with induction of programmed cell death (PCD) type I, apoptosis. However, the mechanisms underlying the antitumor effect of As 2 O 3 on solid tumors are poorly defined. Previously, we reported that As 2 O 3 induced autophagic cell death (PCD type II) but not apoptosis in human malignant glioma cell lines. The purpose of this study was to elucidate the molecular pathway leading to autophagic cell death. In this study, we demonstrated that the cell death was accompanied by involvement of autophagy-specific marker, microtubule-associated protein light chain 3 (LC3), and damage of mitochondrial membrane integrity, but not by caspase activation. Analysis by cDNA microarray, RT-PCR, and Western blot showed that cell death members of Bcl-2 family, Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) and its homologue BNIP3-like (BNIP3L), were upregulated in As 2 O 3 -induced autophagic cell death. Exogenous expression of BNIP3, but not BNIP3L, induced autophagic cell death in malignant glioma cells without As 2 O 3 treatment. When upregulation of BNIP3 induced by As 2 O 3 was suppressed by a dominant-negative effect of the transmembranedeleted BNIP3 (BNIP3DTM), autophagic cell death was inhibited. In contrast, BNIP3 transfection augmented As 2 O 3 -induced autophagic cell death. These results suggest that BNIP3 plays a central role in As 2 O 3 -induced autophagic cell death in malignant glioma cells. This study adds a new concept to characterize the pathways by which As 2 O 3 acts to induce autophagic cell death in malignant glioma cells. Oncogene (2005) 24, 980-991.

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Arsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitro

Cited by 165 publications

References 16 publications

Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels

Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels

Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells

Arsenic trioxide induces autophagic cell death in malignant glioma cells by upregulation of mitochondrial cell death protein BNIP3

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