DNA microarray analysis of human neuroblastoma SH-SY5Y cells exposed to methylmercury

Toyama, Takashi; Yoshida, Eiko; Shinkai, Yasuhiro; Kumagai, Yoshito

doi:10.2131/jts.36.843

Cited by 18 publications

(16 citation statements)

References 5 publications

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“…The biological factors that are altered by MeHg have been explored with the aim of shedding light on the molecular mechanisms that underlie MeHg toxicity (Hwang et al, 2011a(Hwang et al, , 2013aHwang and Naganuma, 2006;Kim et al, 2012Kim et al, , 2013Lee et al, 2012;Takahashi et al, 2013;Toyama et al, 2011). Furthermore, the research group led by Dr. Naganuma has found a large number of proteins that are resistant or hypersensitive to MeHg (Hwang et al, 2007(Hwang et al, , 2010a(Hwang et al, , 2010b(Hwang et al, , 2010c(Hwang et al, , 2011b(Hwang et al, , 2012a(Hwang et al, , 2012b(Hwang et al, , 2013b.…”

Section: Attempts To Identify Cases Of the S-mercuration Of Proteinsmentioning

confidence: 99%

S-Mercuration of cellular proteins by methylmercury and its toxicological implications

2014

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-The accumulation of methylmercury (MeHg) through the daily consumption of large predatory fish poses potential health risks. MeHg has been found to cause Minamata disease, but the full nature of MeHg toxicity remains unclear. Because of its chemical properties, MeHg covalently binds to cellular proteins through their reactive thiols, referred to as S-mercuration, resulting in the formation of protein adducts. In this review, we summarize how the S-mercuration of cellular proteins could be involved in the major mechanisms that have been suggested to underlie MeHg toxicity. Additionally, we introduce our attempts to identify cases of S-mercuration for the research to reveal the true nature of MeHg toxicity.

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Section: Attempts To Identify Cases Of the S-mercuration Of Proteinsmentioning

confidence: 99%

S-Mercuration of cellular proteins by methylmercury and its toxicological implications

2014

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“…Total RNA was extracted from both cell types, and the synthesis of complementary DNA (cDNA) and cRNA labeling were conducted using a Low RNA Fluorescent Linear Amplification kit (Agilent, Palo Alto, CA, USA). Overall changes in gene expression were evaluated using two-color microarray-based gene expression analysis (Hwang et al, 2011;Takeda et al, 2011Takeda et al, , 2013bToyama et al, 2011). Labeled cRNA (Cy3 to control, Cy5 to CBDA) was hybridized to human oligo DNA microarray slides (Agilent) that carried spots for human genes.…”

Section: Preparation Of Total Rna and Dna Microarray Analysesmentioning

confidence: 99%

Down-regulation of cyclooxygenase-2 (COX-2) by cannabidiolic acid in human breast cancer cells

et al. 2014

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-Metastases are known to be responsible for approximately 90% of breast cancer-related deaths. Cyclooxygenase-2 (COX-2) is involved not only in inflammatory processes, but also in the metastasis of cancer cells; it is expressed in 40% of human invasive breast cancers. To comprehensively analyze the effects of cannabidiolic acid (CBDA), a selective COX-2 inhibitor found in the fiber-type cannabis plant (Takeda et al., 2008), on COX-2 expression and the genes involved in metastasis, we performed a DNA microarray analysis of human breast cancer MDA-MB-231 cells, which are invasive breast cancer cells that express high levels of COX-2, treated with CBDA for 48 hr at 25 μM. The results obtained revealed that COX-2 and Id-1, a positive regulator of breast cancer metastasis, were down-regulated (0.19-fold and 0.52-fold, respectively), while SHARP1 (or BHLHE41), a suppressor of breast cancer metastasis, was up-regulated (1.72-fold) and CHIP (or STUB1) was unaffected (1.03-fold). These changes were confirmed by real-time RT-PCR analyses. Taken together, the results obtained here demonstrated that i) CBDA had dual inhibitory effects on COX-2 through down-regulation and enzyme inhibition, and ii) CBDA may possess the ability to suppress genes that are positively involved in the metastasis of cancer cells in vitro.

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“…Total RNA was extracted from both cell types, and complementary DNA (cDNA) synthesis and cRNA labeling were conducted using a Low RNA Fluorescent Linear Amplification Kit (Agilent, Palo Alto, CA, USA). Overall changes in gene expression were evaluated using two-color microarray-based gene expression analysis (Hwang et al, 2011;Takeda et al, 2011Takeda et al, , 2013bToyama et al, 2011). Labeled cRNA (Cy3 to control, Cy5 to (-)-xanthatin) was hybridized to human oligo DNA microarray slides (Agilent) that carried spots for human genes.…”

Section: Preparation Of Total Rna and Dna Microarray Analysesmentioning

confidence: 99%

(–)-Xanthatin induces the prolonged expression of c-Fos through an N-acetyl-L-cysteine (NAC)-sensitive mechanism in human breast cancer MDA-MB-231 cells

et al. 2013

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-We reported that (-)-xanthatin, a xanthanolide sesquiterpene lactone present in the Cocklebur plant, exhibited potent anti-proliferative effects on human breast cancer cells, in which GADD45γ, a novel tumor suppressor gene, was induced. Mechanistically, topoisomerase IIα (Topo IIα) inhibition by (-)-xanthatin was shown to be the upstream trigger that stimulated the expression of GADD45γ mRNA and concomitantly produced reactive oxygen species (ROS) to maintain this expression. Since the anticancer drug etoposide, a selective Topo IIα inhibitor, has also been shown to induce intracellular ROS, (-)-xanthatin may exert its anti-proliferative effects on cancer cells in a similar manner to those of etoposide. In the present study, to generalize its applicability to cancer therapy, we further investigated the biological activities of (-)-xanthatin by comparing its activities to those of the established anti-cancer drug etoposide. After the exposure of breast cancer cells to (-)-xanthatin or etoposide, a prolonged and marked up-regulation in the expression of c-fos, a proapoptotic molecule, was detected together with GADD45γ; and the expression of these molecules was stabilized by ROS and abrogated by the pretreatment with N-acetyl-L-cysteine (NAC), a potent ROS scavenger. (-)-Xanthatin in particular exhibited stronger antiproliferative potential than that of etoposide, which underlies the marked induction of c-fos/GADD45γ and ROS production.

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DNA microarray analysis of human neuroblastoma SH-SY5Y cells exposed to methylmercury

Cited by 18 publications

References 5 publications

<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

Down-regulation of cyclooxygenase-2 (COX-2) by cannabidiolic acid in human breast cancer cells

(–)-Xanthatin induces the prolonged expression of c-Fos through an <i>N</i>-acetyl-L-cysteine (NAC)-sensitive mechanism in human breast cancer MDA-MB-231 cells

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