Oxidative DNA damage is a preliminary step during rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide

Miranda, Sandra Regina; Noguti, Juliana; Carvalho, Juliana Gonçalves; Oshima, Celina T. F.; Ribeiro, Daniel Araki

doi:10.1007/s10735-011-9323-9

Cited by 23 publications

(14 citation statements)

References 28 publications

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“…Therefore, we chose 4NQO model to further investigate these effects in vivo. Oxidative DNA damage is a preliminary step during rat tongue carcinogenesis induced by 4NQO (26). Kohda and colleagues concluded that the 8-OHdG, which was regarded as a major marker of DNA oxidative damage (27,28), can be attributed to 4HAQO-DNA adducts in 4NQO animal model.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus Salivarius REN Inhibits Rat Oral Cancer Induced by 4-Nitroquioline 1-Oxide

Zhang

Wang

Jiang

et al. 2013

Cancer Prevention Research

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Despite significant advances in cancer therapy, cancer-related mobility and mortality are still rising. Alternative strategies such as cancer prevention thus become essential. Probiotics represent an emerging option for cancer prevention, but studies are limited to colon cancers. The efficiency of probiotics in the prevention of other cancers and the correlative mechanism remains to be explored. A novel probiotics Lactobacillus salivarius REN (L. salivarius REN) was isolated from centenarians at Bama of China, which showed highly potent antigenotoxicity in an initial assay. 4-nitroquioline 1-oxide (4NQO)-induced oral cancer model was introduced to study the anticancer activity of L. salivarius REN in vivo. The results indicated that oral administration of probiotic L. salivarius REN or its secretions could effectively suppress 4NQO-induced oral carcinogenesis in the initial and postinitial stage, and the inhibition was in a dose-dependent manner. A significant decrease of neoplasm incidence (65%-0%) was detected in rats fed with the high dose of L. salivarius REN [5 Â 10 10 CFU/kg body weight (bw)/d]. In vivo evidences indicated that the probiotics inhibited 4NQO-induced oral cancer by protecting DNA against oxidative damage and downregulating COX-2 expression. L. salivarius REN treatment significantly decreased the expression of proliferating cell nuclear antigen (PCNA) and induced apoptosis in a dose-dependent manner. Our findings suggest that probiotics may act as potential agents for oral cancer prevention. This is the first report showing the inhibitory effect of the probiotics on oral carcinogenesis. Cancer Prev Res; 6(7); 686-94. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

Lactobacillus Salivarius REN Inhibits Rat Oral Cancer Induced by 4-Nitroquioline 1-Oxide

Zhang

Wang

Jiang

et al. 2013

Cancer Prevention Research

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“…In several types of MPS, previous studies conduced by our research group have revealed changes in biomarkers of oxidative stress, demonstrating lipid peroxidation and protein oxidation, as well as alterations in erythrocyte antioxidant enzymes (Pereira et al 2008(Pereira et al , 2010, suggesting, therefore a possible involvement of reactive oxygen species in these disorders. Intralysosomal GAGs accumulation, directly or indirectly, may cause oxidative imbalance as far as increased cancer risk (Filippon et al 2011b;Miranda et al 2011). We assume that MPS I is able to induce genetic damage in peripheral blood cells as a result of oxidative stress.…”

Section: Resultsmentioning

confidence: 99%

Genomic instability in blood cells from murine model of mucopolysaccharidosis type I

et al. 2011

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Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alfa-iduronidase (IDUA), which leads to intralysosomal accumulation of glycosaminoglycans. Some studies have revealed that oxidative stress plays an important role in MPS I. However, the mechanisms by which these alterations occur are still not fully understood. The aim of this study was to analyze genomic instability in blood cells from murine model of MPS I by single cell gel (comet) assay and micronucleus test. The results pointed out genetic damage in blood cells as depicted by the single cell gel (comet) assay results. By contrast, no increase of micronucleated cells were found in mouse blood cells when compared to negative control. Taken together, our results suggest that IDUA deficiency induces genomic damage in blood cells. Certainly, this finding offers new insights into the mechanisms underlying the relation between IDUA deficiency and clinical manifestations that can occur in MPS I patients.

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“…The medium-term assay is based on the multi-step process of carcinogenesis characterized by initiation, promotion and tumor progression. Chronic administration of 4-NQO in drinking water simulates rat tongue carcinogenesis that mimics the human condition, thus providing an ideal model for studying tumor pathobiology (Ribeiro et al 2004;Miranda et al 2011).…”

Section: W Limmentioning

confidence: 99%

Expression of cancer stem cell marker during 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis

et al. 2014

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One of the theories regarding oral carcinogenesis is that the tumor growth is initiated from cancer stem cells (CSCs) that self-renew and give rise to differentiated tumor cells, like stem cells do in normal tissues. The most common methods of CSC identification are based on CSC marker expression in carcinogenesis. This study examined the expression of CD133 and CD44, the most commonly used CSC biomarkers in oral squamous cell sarcoma (SCC), with the goal of identifying molecular biomarkers whose expression is associated with the multistep oral carcinogenesis. The expression of CD133, CD44, proliferating cell nuclear antigen (PCNA), and Cytokeratin (CK) was examined by Western blot analysis and confirmed by immunohistochemistry in a 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis model. Also, the expression of aldehyde dehydrogenase 1 (ALDH1), OCT-4 and Nanog were investigated for alteration of cancer cell stemness by Western blot. Along with the progress of multistep carcinogenesis, there were slight increases of CD133 and CD44 expression in the dysplasia group compared with normal rats. However, CD133 protein level was significantly overexpressed in SCC. The expression of PCNA and CK were low in normal group, but sequentially increased in SCC. ALDH1, Nanog and OCT-4 expression were significantly increased according to SCC grade during carcinogenesis. The findings indicate that CD133 is useful in identifying oral CSCs, which suggests that CD133 may serve as a predictor to identify CSCs with a high risk of oral cancer development.

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Oxidative DNA damage is a preliminary step during rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide

Cited by 23 publications

References 28 publications

Lactobacillus Salivarius REN Inhibits Rat Oral Cancer Induced by 4-Nitroquioline 1-Oxide

Lactobacillus Salivarius REN Inhibits Rat Oral Cancer Induced by 4-Nitroquioline 1-Oxide

Genomic instability in blood cells from murine model of mucopolysaccharidosis type I

Expression of cancer stem cell marker during 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis

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