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Periostin contributes to arsenic trioxide resistance in hepatocellular carcinoma cells under hypoxia.
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Hypoxia has been suggested to induce chemoresistance in tumor cells. In this study, we aimed to test the hypothesis that hypoxia-inducible factor-1alpha (HIF-1α)/periostin axis might promote arsenic trioxide resistance in hepatocellular carcinoma (HCC) cells under hypoxia. HCC cells were exposed to
Particulate arsenic and iron during anoxia in a eutrophic, urban lake.
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The bioavailability and transport of particle-reactive pollutants are influenced by their partitioning between dissolved and particulate phases. We explored the importance of particle complexation to the arsenic cycle in an urban lake (Upper Mystic Lake, eastern MA, USA) that experiences arsenic
[Effects of arsenic trioxide on apoptosis and proliferation of human lung cancer cells under hypoxia].
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OBJECTIVE
To observe the effects of different concentrations of arsenic trioxide (As(2)O(3)) on apoptosis and proliferation of human lung cancer cell line A549 in vitro under hypoxia and normoxia.
METHODS
A549 cells were treated with 0, 1, 2, 4 micromol/L As2O3 for 12, 24 and 48 h under hypoxia (5%
Multidrug-resistant neuroblastoma cells are responsive to arsenic trioxide at both normoxia and hypoxia.
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Despite intensive treatment, the outcome of high-risk neuroblastoma patients is poor with acquired multidrug resistance as an important cause. Previously, our group has shown that arsenic trioxide (As(2)O(3)) kills multidrug-resistant neuroblastoma cells in vitro and in vivo at clinically tolerable
Hypoxia-simulating agents and selective stimulation of arsenic trioxide-induced growth arrest and cell differentiation in acute promyelocytic leukemic cells.
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OBJECTIVE
We recently reported that hypoxia-mimetic agents cobalt chloride (CoCl2 CoCl2 ) and desferrioxamine (DFO) could induce differentiation of acute myeloid leukemic (AML) cells. Here, we investigate whether these two agents influence the in vitro differentiation-inducing effect of arsenic
Hypoxia-induced exposure of isaza fish to manganese and arsenic at the bottom of Lake Biwa, Japan: experimental and geochemical verification.
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In December 2007, a mass mortality of isaza (Gymnogobius isaza), a goby fish in Lake Biwa, Japan, was observed under severe hypoxia. Considering the level of manganese and arsenic in the dead isaza during the event was much higher than that in live isaza, hypoxia-induced mobilization of manganese
Ethanol enhances tumor angiogenesis in vitro induced by low-dose arsenic in colon cancer cells through hypoxia-inducible factor 1 alpha pathway.
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Health effects due to environmental exposure to arsenic are a major global health concern. Arsenic has been known to induce carcinogenesis and enhance tumor development via complex and unclear mechanism. Ethanol is also a well-established risk factor for many malignancies. However, little is known
Interference between arsenic-induced toxicity and hypoxia.
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Plants often face combinatorial stresses in their natural environment. Here, arsenic (As) toxicity was combined with hypoxia (Hpx) in the roots of Arabidopsis thaliana as it often occurs in nature. Arsenic inhibited growth of both roots and leaves, whereas root growth almost entirely ceased in Hpx.
Arsenic trioxide inhibits the growth of human lung cancer cell lines via cell cycle arrest and induction of apoptosis at both normoxia and hypoxia.
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Arsenic trioxide (As(2)O(3)) has been established to be an effective agent for treating acute promyleocytic leukemia. Laboratory data suggest that As(2)O(3) induces apoptosis of several solid tumor cells including lung cancer cells. Regions of tissue hypoxia often arise in aggressive solid tumors,
Normoxically overexpressed hypoxia inducible factor 1-alpha is involved in arsenic trioxide resistance acquisition in hepatocellular carcinoma.
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BACKGROUND
The aim of this study was to examine the underlying signaling mechanisms of arsenic trioxide (ATO)-mediated anticancer effects and the responsible biomarker(s) for the acquired resistance in human heptatocellular carcinoma (HCC).
METHODS
The therapeutic effects of ATO were examined using
Retraction: "Ethanol Enhances Tumor Angiogenesis In Vitro Induced by Low-Dose Arsenic in Colon Cancer Cells Through Hypoxia-Inducible Factor 1 Alpha Pathway".
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Hypoxia-simulating agents selectively stimulate arsenic trioxide-induced growth arrest and cell differentiation in acute promyelocytic leukemic cells.
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[Glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activity in arsenic poisoning and in hypoxemia caused by sodium nitrite].
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Effect of arsenic compounds on resistance of the central nervous system of the rat to hypoxia and anoxia during ontogenesis.
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Metallothionein 3 Is a Hypoxia-Upregulated Oncogene Enhancing Cell Invasion and Tumorigenesis in Human Bladder Carcinoma Cells.
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Metallothioneins have been viewed as modulators in a number of biological regulations regarding cancerous development; however, the function of metallothionein 3 (MT3) in bladder cancer is unexplored. We determined the regulatory mechanisms and potential function of MT3 in bladder carcinoma
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