DEACL - Departamento de Análises Clínicas

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Browsing DEACL - Departamento de Análises Clínicas by Subject "Allyl isothiocyanate"

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    Cell cycle kinetics, apoptosis rates, DNA damage and TP53 geneexpression in bladder cancer cells treated with allyl isothiocyanate(mustard essential oil).
    (2014) Sávio, André Luiz Ventura; Silva, Glenda Nicioli da; Camargo, Elaine Aparecida de; Salvadori, Daisy Maria Fávero
    Allyl isothiocyanate (AITC) is present in plants of the cruciferous family and is abundant in mustard seed.Due to its high bioavailability in urine after ingestion, AITC has been considered a promising antineoplasticagent against bladder cancer. Because TP53 mutations are the most common alterations in bladder cancercells and are frequently detected in in situ carcinomas, in this study, we investigated whether the AITCeffects in bladder cancer cells are dependent on the TP53 status. Two bladder transitional carcinoma celllines were used: RT4, with wild-type TP53; and T24, mutated TP53 gene. AITC was tested at concentrationsof 0.005, 0.0625, 0.0725, 0.0825, 0.0925, 0.125 and 0.25 _M in cytotoxicity, cell and clonogenic survivalassays, comet and micronucleus assays and for its effects on cell cycle and apoptosis by flow cytometry andon TP53 gene expression. The data showed increased primary DNA damage in both cell lines; however,lower concentrations of AITC were able to induce genotoxicity in the mutant cells for the TP53 gene.Furthermore, the results demonstrated increased apoptosis and necrosis rates in the wild-type cells, butnot in mutated TP53 cells, and cell cycle arrest in the G2 phase for mutated cells after AITC treatment.No significant differences were detected in TP53 gene expression in the two cell lines. In conclusion,AITC caused cell cycle arrest, increased apoptosis rates and varying genotoxicity dependent on the TP53status. However, we cannot rule out the possibility that those differences could reflect other intrinsicgenetic alterations in the examined cell lines, which may also carry mutations in genes other than TP53.Therefore, further studies using other molecular targets need to be performed to better understand themechanisms by which AITC may exert its antineoplastic properties against tumor cells.
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    Inhibition of bladder cancer cell proliferation by allyl isothiocyanate(mustard essential oil).
    (2015) Sávio, André Luiz Ventura; Silva, Glenda Nicioli da; Salvadori, Daisy Maria Fávero
    Natural compounds hold great promise for combating antibiotic resistance, the failure to control somediseases, the emergence of new diseases and the toxicity of some contemporary medical products. Allylisothiocyanate (AITC), which is abundant in cruciferous vegetables and mustard seeds and is commonlyreferred to as mustard essential oil, exhibits promising antineoplastic activity against bladder cancer,although its mechanism of action is not fully understood. Therefore, the aim of this study was to inves-tigate the effects of AITC activity on bladder cancer cell lines carrying a wild type (wt; RT4) or mutated(T24) TP53 gene. Morphological changes, cell cycle kinetics and CDK1, SMAD4, BAX, BCL2, ANLN and S100Pgene expression were evaluated. In both cell lines, treatment with AITC inhibited cell proliferation (at62.5, 72.5, 82.5 and 92.5 _M AITC) and induced morphological changes, including scattered and elon-gated cells and cellular debris. Gene expression profiles revealed increased S100P and BAX and decreasedBCL2 expression in RT4 cells following AITC treatment. T24 cells displayed increased BCL2, BAX and ANLNand decreased S100P expression. No changes in SMAD4 and CDK1 expression were observed in either cellline. In conclusion, AITC inhibits cell proliferation independent of TP53 status. However, the mechanismof action of AITC differed in the two cell lines; in RT4 cells, it mainly acted via the classical BAX/BCL2 path-way, while in T24 cells, AITC modulated the activities of ANLN (related to cytokinesis) and S100P. Thesedata confirm the role of AITC as a potential antiproliferative compound that modulates gene expressionaccording to the tumor cell TP53 genotype.