Acquisition of apoptotic resistance in arsenic-induced malignant transformation: role of the JNK signal transduction pathway

Qu, Wei; Bortner, Carl D.; Sakurai, Takeshi; Hobson, Michael J.; Waalkes, Michael P.

doi:10.1093/carcin/23.1.151

Cited by 61 publications

(47 citation statements)

References 33 publications

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“…In contrast, more recent data from animal models have shown the possibility of a strong bond with liver tumor formation [261][262][263][264][265][266][267][268] . Various carcinogenic mechanisms, genetic and epigenetic, have been proposed: DNA methylation, oxidative damage, genomic instability and reduction of programmed cell death [269][270][271][272][273][274] .…”

Section: Arsenicmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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Hepatocellular carcinoma (HCC) is the most common type of liver cancer. The main risk factors for HCC are alcoholism, hepatitis B virus, hepatitis C virus, nonalcoholic steatohepatitis, obesity, type 2 diabetes, cirrhosis, aflatoxin, hemochromatosis, Wilson's disease and hemophilia. Occupational exposure to chemicals is another risk factor for HCC. Often the relationship between occupational risk and HCC is unclear and the reports are fragmented and inconsistent. This review aims to summarize the current knowledge regarding the association of infective and non-infective occupational risk exposure and HCC in order to encourage further research and draw attention to this global occupational public health problem. Core tip: Hepatocellular carcinoma (HCC) is the fifth most common human cancer. This review summarizes current knowledge regarding the occupational risk factors of HCC. In particular, we underline not only the infective but also non-infective occupational risk exposure, including chemical agents and toxic metabolites which are a major cause of liver damage.

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Section: Arsenicmentioning

confidence: 99%

Hepatocellular carcinoma and the risk of occupational exposure

Rapisarda

Loreto

Malaguarnera

et al. 2016

WJH

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“…MAPKs comprise a family of serine/threonine phosphorylating proteins that mediate a variety of signal transduction pathways [22,26]. Of the major MAPKs, the c-Jun NH 2 -terminal kinases (JNKs) result in stress responses, growth arrest, and/or apoptosis [22].…”

Section: Discussionmentioning

confidence: 99%

“…Of the major MAPKs, the c-Jun NH 2 -terminal kinases (JNKs) result in stress responses, growth arrest, and/or apoptosis [22]. Arsenic can induce JNKs activity in various cells [22,26] and activation of JNK by arsenic contributes to apoptosis [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…Arsenic can induce JNKs activity in various cells [22,26] and activation of JNK by arsenic contributes to apoptosis [27,28]. Interestingly, arsenic-transformed cells become highly resistant to arsenic-induced apoptosis from the perturbation of JNK1/2 activity [22]. Thus, the JNK pathway appears to play an important role in arsenic-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…The kinase reaction was performed by adding 100 μM of ATP to the suspension. Phosphorylation of c-Jun was measured by western blot analysis with a phospho-specific c-Jun antibody that specifically detects Ser63-phosphorylated c-Jun, a site important for c-Jun-dependent transcriptional activity [22]. Since this assay measures the end-product of an enzymatic reaction, activity can be compared across groups based on the use of equal amounts of total cellular protein.…”

Section: Jnk Activity Assaymentioning

confidence: 99%

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The nitric oxide prodrug, V-PYRRO/NO, mitigates arsenic-induced liver cell toxicity and apoptosis

Liu

Fuquay

et al. 2007

Cancer Letters

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Arsenite is an important cancer chemotherapeutic. The liver is a major target tissue of arsenic toxicity and hepatotoxicity may limit its chemotherapeutic efficacy. O 2 -vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO) is a liver-selective nitric oxide (NO)-producing prodrug metabolized by hepatic P450 enzymes to release NO locally. V-PYRRO/NO protects against various organic or inorganic hepatotoxicants but any role in arsenic hepatotoxicity is undefined. Thus, we studied the effects of V-PYRRO/NO (0-1000 μM) pretreatment on inorganic arsenic-induced toxicity in cultured rat liver (TRL 1215) cells. These cells metabolized the prodrug to release NO, producing extracellular nitrite levels to 41.7-fold above control levels (7.50 ± 0.38 μM) after 24 h V-PYRRO/ NO (1000 μM) exposure. The effect of pretreatment with V-PYRRO/NO (24 h) on the cytolethality of arsenic (as NaAsO 2 ) exposure (24 h) was assessed. Arsenic was markedly less toxic in V-PYRRO/ NO pretreated cells (LC 50 = 30.3 μM) compared to control (LC 50 = 20.1 μM) and the increases in LC 50 showed a direct relationship to the level of NO produced (measured as nitrite). Consistent with the cytolethality data, V-PYRRO/NO pretreatment markedly reduced arsenic-induced apoptosis as assessed by DNA fragmentation. Activation of the c-Jun N-terminal kinase (JNK) pathway can be critical to apoptosis and pretreatment with V-PYRRO/NO suppressed arsenic-induced JNK activation. V-PYRRO/NO pretreatment modestly increased metallothionein (MT), a metal-binding protein, but greatly enhanced arsenic induction of MT. Thus, V-PYRRO/NO pretreatment directly mitigates arsenic toxicity in cultured liver cells, reducing cytolethality, apoptosis and related JNK pathway activation, apparently through generation of NO. The role of NO in reducing the hepatotoxicity of arsenical chemotherapeutics in vivo deserves additional study.

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Epoxy‐montmorillonite clay nanocomposites: Synthesis and characterization

Nigam

Setua

Mathur

et al. 2004

J of Applied Polymer Sci

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Nanocomposites of epoxy resin with montmorillonite clay were synthesized by swelling of different proportions of the clay in a diglycidyl ether of bisphenol-A followed by in situ polymerization with aromatic diamine as a curing agent. The montmorillonite was modified with octadecylamine and made organophilic. The organoclay was found to be intercalated easily by incorporation of the epoxy precursor and the clay galleries were simultaneously expanded. However, Na-montmorillonite clay could not be intercalated during the mixing or through the curing process. Curing temperature was found to provide a balance between the reaction rate of the epoxy precursor and the diffusion rate of the curing agent into the clay galleries. The cure kinetics were studied by differential scanning calorimetry. The exfoliation behavior of the organoclay system was investigated by X-ray diffraction. Thermogravimetric analysis was used to determine the thermal stability, which was correlated with the ionic exchange between the organic species and the silicate layers. The morphology of the nanocomposites was evaluated by scanning electron microscopy.

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Acquisition of apoptotic resistance in arsenic-induced malignant transformation: role of the JNK signal transduction pathway

Cited by 61 publications

References 33 publications

Hepatocellular carcinoma and the risk of occupational exposure

Hepatocellular carcinoma and the risk of occupational exposure

The nitric oxide prodrug, V-PYRRO/NO, mitigates arsenic-induced liver cell toxicity and apoptosis

Epoxy‐montmorillonite clay nanocomposites: Synthesis and characterization

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