The alteration of mitochondria is an early event of arsenic trioxide induced apoptosis in esophageal carcinoma cells.

Shen, Zhong-Ying; Shen, Jianxin; Cai, Wenfeng; Hong, Chao‐Qun; Zheng, Maochao

doi:10.3892/ijmm.5.2.155

Cited by 55 publications

(52 citation statements)

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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: 67%

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: 67%

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: 66%

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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“…36 In another report, the apoptosis of leukemia U937 cells induced by As 2 O 3 was dependent on the activation of p38, inactivation of ERK and the Ca 21 -dependent production of superoxide. 37 The anticancer activity of As 2 O 3 is in part related to its effects on mitochondria, 38,39 and the generation of nitric oxide and ROS. 40,41 Accordingly, As 2 O 3 exerts antitumor effects as a result of its highly cytotoxic nature.…”

Section: Discussionmentioning

confidence: 99%

Arsenic trioxide synergizes with B7H3‐mediated immunotherapy to eradicate hepatocellular carcinomas

Luo

Qiao

Meng

et al. 2005

Intl Journal of Cancer

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Arsenic trioxide (As 2 O 3 ), a valuable anticancer drug for the treatment of acute promyelocytic leukemia, may also have therapeutic potential for the treatment of solid tumors. However, its therapeutic efficacy against solid tumors is lacking even at high dosages. Other therapeutic strategies are required to enhance the efficacy of As 2 O 3 against solid tumors such as hepatocellular carcinoma (HCC), which is refractory to chemotherapy. B7H3, a new member of the B7 family, has been shown to induce antitumor immunity. Intratumoral injection of B7H3 plasmids eradicates small EL-4 lymphomas, but monotherapy is ineffective against large tumors. Here we investigated whether As 2 O 3 would synergize with B7H3 immunotherapy to combat HCC. Large subcutaneous H22 HCCs (0.7-0.8 cm in diameter) established in BALB/c mice were rapidly and completely eradicated when intratumoral administration of As 2 O 3 was preceded by in situ gene transfer of B7H3. In contrast, neither As 2 O 3 nor B7H3 monotherapy was effective. The antitumor activity of As 2 O 3 was attributed to increased tumor-cell apoptosis, perhaps as a result of direct cytotoxicity as well as decreased tumor angiogenesis. Combination therapy generated potent systemic antitumor immunity mediated by CD81 and NK cells that was effective in combating a systemic challenge of 1 3 10 7 parental H22 cells. It led to the simultaneous and complete regression of multiple distant tumor nodules, concomitant with increased levels of serum IFN-c and cytotoxic T lymphocyte (CTL) activity. In conclusion, combining B7H3-mediated immunotherapy with As 2 O 3 warrants investigation as a therapeutic strategy to combat HCC, and other malignancies. ' 2005 Wiley-Liss, Inc.

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The alteration of mitochondria is an early event of arsenic trioxide induced apoptosis in esophageal carcinoma cells.

Cited by 55 publications

References 0 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 synergizes with B7H3‐mediated immunotherapy to eradicate hepatocellular carcinomas

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