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首页> 外文期刊>Cellular Physiology and Biochemistry >The Epigenetic Factor KDM2B Regulates EMT and Small GTPases in Colon Tumor Cells
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The Epigenetic Factor KDM2B Regulates EMT and Small GTPases in Colon Tumor Cells

机译：表观遗传因子KDM2B调节结肠肿瘤细胞中的EMT和小GTPase。

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Background/Aims The epigenetic factor KDM2B is a histone demethylase expressed in various tumors. Recently, we have shown that KDM2B regulates actin cytoskeleton organization, small Rho GTPases signaling, cell-cell adhesion and migration of prostate tumor cells. In the present study, we addressed its role in regulating EMT and small GTPases expression in colon tumor cells. Methods We used RT-PCR for the transcriptional analysis of various genes, Western blotting for the assessment of protein expression and immunofluorescence microscopy for visualization of fluorescently labeled proteins. Results We report here that KDM2B regulates EZH2 and BMI1 in HCT116 colon tumor cells. Knockdown of this epigenetic factor induced potent up-regulation of the protein levels of the epithelial markers E-cadherin and ZO-1, while the mesenchymal marker N-cadherin was downregulated. On the other hand, KDM2B overexpression downregulated the levels of both epithelial markers and upregulated the mesenchymal marker, suggesting control of EMT by KDM2B. In addition, RhoA, RhoB and RhoC protein levels diminished upon KDM2B-knockdown, while all three small GTPases became upregulated in KDM2B-overexpressing HCT116 cell clones. Interestingly, Rac1 GTPase level increased upon KDM2B-knockdown and diminished in KDM2B-overexpressing HCT116 colon tumor- and DU-145 prostate cancer cells. Conclusions These results establish a clear functional role of the epigenetic factor KDM2B in the regulation of EMT and small-GTPases expression in colon tumor cells and further support the recently postulated oncogenic role of this histone demethylase in various tumors.
机译：背景/目的表观遗传因子KDM2B是在多种肿瘤中表达的组蛋白脱甲基酶。最近，我们已经显示KDM2B调节肌动蛋白的细胞骨架组织，小Rho GTPases信号传导，细胞粘附和前列腺肿瘤细胞的迁移。在本研究中，我们探讨了其在结肠癌细胞中调控EMT和小GTPases表达的作用。方法我们使用RT-PCR进行各种基因的转录分析，使用Western印迹法评估蛋白质表达，并使用免疫荧光显微镜观察荧光标记的蛋白质。结果我们在这里报告KDM2B调节HCT116结肠肿瘤细胞中的EZH2和BMI1。抑制这种表观遗传因子可诱导上皮标记物E-cadherin和ZO-1的蛋白质水平有效上调，而间充质标记物N-cadherin则被下调。另一方面，KDM2B的过表达下调了两个上皮标志物的水平，并上调了间充质标志物，表明KDM2B对EMT的控制。此外，在KDM2B敲低后，RhoA，RhoB和RhoC蛋白水平降低，而所有三个小GTPases在过表达KDM2B的HCT116细胞克隆中上调。有趣的是，Rac1 GTPase水平在KDM2B敲低后增加，并在过表达KDM2B的HCT116结肠肿瘤和DU-145前列腺癌细胞中减少。结论这些结果建立了表观遗传因子KDM2B在结肠肿瘤细胞EMT和小GTPases调控中的明确功能作用，并进一步支持了该组蛋白脱甲基酶最近在各种肿瘤中的致癌作用。

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