首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Activation of the Wnt/beta-catenin signaling pathway during oral carcinogenesis process is not influenced by the absence of galectin-3 in mice.
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Activation of the Wnt/beta-catenin signaling pathway during oral carcinogenesis process is not influenced by the absence of galectin-3 in mice.

机译:口腔癌发生过程中Wnt /β-catenin信号通路的激活不受小鼠中galectin-3缺失的影响。

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BACKGROUND/AIM: Galectin-3 has been associated with activated Wnt pathway, translocating beta-catenin into the nucleus. However, it is still unknown whether this lectin drives the Wnt signaling activation in lesions from galectin-3-deficient (Gal3/) mice. The purpose was to study beta-catenin expression in tongue lesions from Gal3/ and wild-type (Gal3/) mice and the status of Wnt signaling. MATERIALS AND METHODS: Twenty Gal3/ and Gal3/ male mice were challenged with 4-nitroquinolin-1-oxide and killed at week 16 and 32. Tongues were processed and stained with H&E to detect dysplasias and carcinomas. An imunohistochemical assay was performed to evaluate beta-catenin expression. RESULTS: Carcinomas were more evident in Gal3/ than Gal3/ mice (55.5% vs. 28.5%, respectively; p>0.05). Elevated expression of non-membranous beta-catenin was observed in dysplasias and carcinomas from both groups (p>0.05). CONCLUSION: Absence of galectin-3 does not interfere in the pattern of beta-catenin expression and therefore in the mediation of the Wnt signaling pathway.
机译:背景/目的:Galectin-3已与激活的Wnt途径相关联,将β-catenin转运到细胞核中。但是,尚不知道这种凝集素是否会在半乳糖凝集素3缺失(Gal3 /)小鼠的病变中驱动Wnt信号激活。目的是研究来自Gal3 /和野生型(Gal3 /)小鼠的舌苔中β-catenin的表达以及Wnt信号的状态。材料与方法:20只Gal3 /和Gal3 /雄性小鼠用4-硝基喹啉-1-氧化物攻击并在第16和32周处死。对舌头进行处理并用H&E染色以检测异型增生和癌变。进行免疫组织化学测定以评估β-连环蛋白表达。结果:Gal3 /小鼠比Gal3 /小鼠更明显(分别为55.5%和28.5%; p> 0.05)。两组的异型增生和癌组织中非膜性β-catenin的表达均升高(p> 0.05)。结论:缺乏galectin-3不会干扰β-catenin的表达模式,因此不会干扰Wnt信号通路的介导。

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