Arsenic trioxide induces apoptosis of human gastrointestinal cancer cells

Ma, Zongwen; Xu, Hongyu; Jiang, Miao; Yang, Youlin; Liu, Lianxin; Li, Yinghua

doi:10.3748/wjg.v20.i18.5505

Cited by 17 publications

(6 citation statements)

References 15 publications

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“…So we can anticipate a multilayer and deeper understanding of the MOA of ATO's antitumor activity when the metabolomics data are combined with other systematic data, such as genomics, transcriptomics, and proteomics. Several studies have shown that ATO perturbation in solid tumor may have different mechanisms from that of hematological carcinoma [34][35][36][37]. According to our recent study [38], ATO binds to >300 proteins.…”

Section: Discussionmentioning

confidence: 99%

Construction of a metabolomics profile of arsenic trioxide effect in gastric carcinoma cell line SGC7901

Chen¹,

Zhang

Yang

et al. 2016

ABBS

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Arsenic trioxide (ATO) is highly effective for treating acute promyelocytic leukemia. It also holds the promise for treating solid tumors, including gastric carcinoma. However, the molecular mechanism of the effectiveness of ATO to solid tumor is still poorly understood. In this study, we chosed gastric carcinoma as an example and tried to reveal the antitumor mechanism through metabolomics. Gastric carcinoma cell line SGC7901 was treated with ATO for 6, 12, and 24 h. The global metabolite profiles were monitored by metabolomics analysis using gas chromatography (GC)/mass spectrometry (MS) and liquid chromatography/MS/MS. A total of 281 certified metabolites were reliably detected. Bioinformatics analysis showed that glycerophospholipid synthesis, one-carbon synthesis, and glutathione synthesis were affected dramatically. Other cellular functions/pathways that had been affected included inflammatory response, nicotinamide adenine dinucleotide (NAD + ), and polyamine biosynthesis pathway. The metabolomics data from this study, in combination with previous transcriptomics and proteomics data, could serve as valuable resources for the understanding of the specific antitumor mechanism of ATO treatment.

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Section: Discussionmentioning

confidence: 99%

Construction of a metabolomics profile of arsenic trioxide effect in gastric carcinoma cell line SGC7901

Chen¹,

Zhang

Yang

et al. 2016

ABBS

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“…Whereas evidence suggests that arsenic can activate the PI3K/AKT/mTOR pathway and stimulating cell proliferation in normal, cells such as BEAS2B and SV-HUC-1, the opposite phenomenon seems to occur in cancerous cells. Specifically, arsenic induces apoptosis to varying degrees in different types of cancer cells, such as human colorectal adenocarcinoma cell (HT-29) colon, neuroblastoma, prostate, B-cell leukemia, and gastrointestinal cancer cells ( Akao et al, 1999 ; Cha et al, 2006 ; Ma et al, 2014 ; You et al, 2015 ; Stevens et al, 2017 ). In most of these studies, arsenic trioxide is used instead of sodium arsenite or arsenic trichloride, which are typically used for treatment of noncarcinoma cell studies (see Tables 1 and 2 ).…”

Section: Introductionmentioning

confidence: 99%

PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis

Chen

Costa

2018

Mol Pharmacol

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Arsenic is a naturally occurring, ubiquitous metalloid found in the Earth’s crust. In its inorganic form, arsenic is highly toxic and carcinogenic and is widely found across the globe and throughout the environment. As an International Agency for Research on Cancer–defined class 1 human carcinogen, arsenic can cause multiple human cancers, including liver, lung, urinary bladder, skin, kidney, and prostate. Mechanisms of arsenic-induced carcinogenesis remain elusive, and this review focuses specifically on the role of the PI3K/AKT/mTOR pathway in promoting cancer development. In addition to exerting potent carcinogenic responses, arsenic is also known for its therapeutic effects against acute promyelocytic leukemia. Current literature suggests that arsenic can achieve both therapeutic as well as carcinogenic effects, and this review serves to examine the paradoxical effects of arsenic, specifically through the PI3K/AKT/mTOR pathway. Furthermore, a comprehensive review of current literature reveals an imperative need for future studies to establish and pinpoint the exact conditions for which arsenic can, and through what mechanisms it is able to, differentially regulate the PI3K/AKT/mTOR pathway to maximize the therapeutic and minimize the carcinogenic properties of arsenic.

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“…It is well documented that arsenic trioxide (As 2 O 3 ) exerts antitumor effect in several cancers including leukemia [ 5 ], breast cancer [ 6 ], prostate cancer [ 7 ], lung cancer [ 8 ], cervical cancer [ 9 ], gastric cancer [ 10 , 11 ], pancreatic cancer [ 12 ], hepatocellular cancer [ 13 ] and glioblastoma [ 14 ]. Thus, Trisenox as a trade name of arsenic trioxide from Cephalon Biopharmaceutical Company has been applied to treat acute promyelocytic leukemia (APL) as a chemotherapeutic agent approved by the US FDA [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of STAT3/VEGF/CDK2 axis signaling is critically involved in the antiangiogenic and apoptotic effects of arsenic herbal mixture PROS in non-small lung cancer cells

Lee

Bae³

et al. 2017

Oncotarget

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Arsenic trioxide induces apoptosis of human gastrointestinal cancer cells

Abstract: These results demonstrate that As₂O₃ treatment in patients with gastrointestinal cancers can induce apoptosis in gastrointestinal cancer cells and down-regulate Bcl-2 protein expression.

Cited by 17 publications

References 15 publications

Construction of a metabolomics profile of arsenic trioxide effect in gastric carcinoma cell line SGC7901

Construction of a metabolomics profile of arsenic trioxide effect in gastric carcinoma cell line SGC7901

PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis

Inhibition of STAT3/VEGF/CDK2 axis signaling is critically involved in the antiangiogenic and apoptotic effects of arsenic herbal mixture PROS in non-small lung cancer cells

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