Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calmodulin (CaM), the principal mediator of the calcium signal, regulates numerous processes pertinent to neural function. Mammalian CaM is generated from three genes that give rise to five distinct transcripts. To determine the regulation of individual CaM transcripts in neurons, we assessed their abundance during differentiation of human IMR-32 neuroblastoma cells. Northern analysis revealed that the 4.1 kb CALM1 transcript was specifically upregulated about two-fold during differentiation, and that this increase correlated with neurite extension. By contrast, the CALM2 and CALM3 mRNAs as well as the 1.7 kb CALM1 transcript showed an initial increase but then returned to levels close to, or only slightly above, controls. The increase in the 4.1 kb transcript was largely due to its specific stabilization in differentiated cells. However, total cellular CaM levels did not change significantly throughout differentiation. To begin to address whether the 4.1 kb CALM1 transcript might play a unique role in providing local CaM pools, we determined its localization in differentiated IMR-32 cells using in situ hybridization. The 4.1 kb CALM1 transcript localized to the cell body, but was also present within extending neurites. This finding agrees with in vivo studies showing elevated levels of the 4.1 kb CALM1 transcript in adult rat central neurons and the presence of CALM1 transcripts in dendrites, and establishes a human in vitro model system to study individual CaM transcripts with respect to neuronal functions.
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PMID:Regulation of calmodulin mRNAs in differentiating human IMR-32 neuroblastoma cells. 1244 64

Okadaic acid (OA) is one of the most common and highly distributed marine toxins. It can be accumulated in several molluscs and other marine organisms and cause acute gastrointestinal symptoms after oral consumption by humans, called diarrheic shellfish poisoning. However other toxic effects beyond these gastrointestinal symptoms were also reported. Thus, OA was found to induce important chromosomal abnormalities and other genetic injuries that can lead to severe pathologies, including cancer. Furthermore, the relationship between OA and carcinogenic processes has been previously demonstrated in in vivo studies with rodents, and also suggested in human epidemiological studies. In this context, further research is required to better understand the underlying mechanisms of OA-related tumourigenesis. In a previous study, we identified 247 genes differentially expressed in SHSY5Y neuroblastoma cells exposed to 100nM OA at different times (3, 24 and 48h) by means of suppression subtractive hybridization. These genes were involved in relevant cell functions such as signal transduction, cell cycle, metabolism, and transcription and translation processes. However, due to the high potential percentage of false positives that may be obtained by this approach, results from SSH are recommended to be analyzed by an independent method. In the present study, we selected ten genes related to cancer initiation or progression, directly or indirectly, for further quantitative PCR analysis (ANAPC13, PTTG1, CALM2, CLU, HN1, MALAT1, MAPRE2, MLLT11, SGA-81M and TAX1BP1). Results obtained showed important alterations in the expression patterns of all the genes evaluated at one or more treatment times, providing, for the first time, a possible explanation at the molecular level of the potential relationship between the consumption of OA-contaminated shellfish and the incidence of different cancers in humans. Nevertheless, given the complexity of this process, more exhaustive studies are required before drawing any final conclusion.
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PMID:The marine toxin okadaic acid induces alterations in the expression level of cancer-related genes in human neuronal cells. 2356 Dec 63

Plant phenolics have shown to activate apoptotic cell death in different tumourigenic cell lines. In this study, we evaluated the effects of juniper berry extract (Juniperus communis L.) on p53 protein, gene expression and DNA fragmentation in human neuroblastoma SH-SY5Y cells. In addition, we analyzed the phenolic composition of the extract. We found that juniper berry extract activated cellular relocalization of p53 and DNA fragmentation-dependent cell death. Differentially expressed genes between treated and non-treated cells were evaluated with the cDNA-RDA (representational difference analysis) method at the early time point of apoptotic process when p53 started to be activated and no caspase activity was detected. Twenty one overexpressed genes related to cellular stress, protein synthesis, cell survival and death were detected. Interestingly, they included endoplasmic reticulum (ER) stress inducer and sensor HSPA5 and other ER stress-related genes CALM2 and YKT6 indicating that ER stress response was involved in juniper berry extract mediated cell death. In composition analysis, we identified and quantified low concentrations of fifteen phenolic compounds. The main groups of them were flavones, flavonols, phenolic acids, flavanol and biflavonoid including glycosides of quercetin, apigenin, isoscutellarein and hypolaetin. It is suggested that juniper berry extract induced the p53-associated apoptosis through the potentiation and synergism by several phenolic compounds.
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PMID:Cellular Stress and p53-Associated Apoptosis by Juniperus communis L. Berry Extract Treatment in the Human SH-SY5Y Neuroblastoma Cells. 2742 50