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Malabsorption is a major and common clinical characteristics of short bowel syndrome (SBS) and inflammatory bowel diseases (IBD). Traditional treatment opportunities have focused on decreasing malabsorptive losses via dietary modifications and antisecretory/antidiarrheal agents. However, novel therapeutic modalities aim to enhance the absorptive capacity of the residual bowel by the administration of different intestinal growth factors including teduglutide. In a current study the existence of two distinct functional putative epithelial stem cell subpopulations (i.e. Lgr5+/Bmi1? and Lgr5?/Bmi1+) have been described in a rat model of ileal resection and anastomosis. The described epithelial stem cell subpopulations displayed distinct behaviour after surgical injury and teduglutide administration. Though teduglutide was found to be clinically effective, we must keep in mind that growth factors theoretically may provoke adenoma development and subsequent malignant transformation. The present results give us a better insight into the role of stem cell modulation in intestinal repair. Based on these results new perioperative adjuvant pharmacological approaches may be developed for SBS and IBD patients to reduce the clinical symptoms and complications of associated malabsorption. 相似文献
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Wen Deng Yuan Zhou Agnes F.Y. Tiwari Hang Su Jie Yang Dandan Zhu Victoria Ming Yi Lau Pok Man Hau Yim Ling Yip Annie L.M. Cheung Xin‐Yuan Guan Sai Wah Tsao 《International journal of cancer. Journal international du cancer》2015,136(6):1361-1370
Apart from regulating stem cell self‐renewal, embryonic development and proliferation, Bmi‐1 has been recently reported to be critical in the maintenance of genome integrity. In searching for novel mechanisms underlying the anticlastogenic function of Bmi‐1, we observed, for the first time, that Bmi‐1 positively regulates p21 expression. We extended the finding that Bmi‐1 deficiency induced chromosome breaks in multiple cancer cell models. Interestingly, we further demonstrated that knockdown of cyclin E or ectopic overexpression of p21 rescued Bmi‐1 deficiency‐induced chromosome breaks. We therefore conclude that p21/cyclin E pathway is crucial in modulating the anticlastogenic function of Bmi‐1. As it is well established that the overexpression of cyclin E potently induces genome instability and p21 suppresses the function of cyclin E, the novel and important implication from our findings is that Bmi‐1 plays an important role in limiting genomic instability in cylin E‐overexpressing cancer cells by positive regulation of p21. 相似文献
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Jin‐Qiu Feng Zi‐Yuan Xu Lin‐Jun Shi Lan Wu Wei Liu Zeng‐Tong Zhou 《Journal of oral pathology & medicine》2013,42(2):148-153
J Oral Pathol Med (2013) 42 : 148–153 Background: Oral erythroplakia (OE) is a notoriously aggressive oral pre‐malignant lesion with a high tendency to oral cancer development, but its biological behavior is largely unknown. The objective of this study was to determine the expression of cancer stem cell markers ALDH1 and Bmi1 in OE and their correlation with malignant transformation of OE. Methods: In a retrospective case–control study, expression patterns of ALDH1 and Bmi1 were determined using immunohistochemistry in samples from 34 patients with OE, including patients with untransformed lesions (n = 17) and patients with malignant transformed lesions (n = 17). Results: ALDH1 and Bmi1 expression was observed in 19 (55.9%) and 20 (58.8%) of 34 patients with OE, respectively. Multivariate analysis revealed that ALDH1 expression was significantly associated with increased risk of transformation (P < 0.05), but Bmi1 expression was not a significant marker (P > 0.05). Notably, the coexpression of both ALDH1 and Bmi1 was a strong indicator associated with 8.56‐fold (95% confidence interval [CI], 1.74–42.17; P < 0.01) for malignant transformation. Point prevalence analysis revealed that 78.6% (95% CI, 54.0–100) of the patient with coexpression of both ALDH1 and Bmi1 developed oral cancer. Conclusion: Our data indicated that the expression patterns of ALDH1 and Bmi1 in OE were associated with malignant transformation, suggesting that they may be valuable predictors for evaluating the risk of oral cancer. 相似文献
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目的: 探讨Bmi1如何调控舌鳞癌侧群细胞的迁移、侵袭和增殖能力。 方法: 首先采用Hoechst33342法,利用流式细胞仪分选舌鳞癌细胞株UM1(高转移株)中的侧群细胞(side population cell, SP)和非侧群细胞(non-side population cell, Non-SP)。Transwell 实验检测沉默Bmi1后SP细胞的迁移、侵袭能力。球囊形成和平板克隆实验检测沉默Bmi1后SP细胞的球囊和克隆形成率;CCK8 实验检测沉默Bmi1后SP细胞的增殖能力。Western免疫印迹检测沉默Bmi1后SP细胞中侵袭、转移相关基因(SOD2、Slug)及干细胞标志物(ABCG2、Nanog)的表达水平。采用SPSS17.0软件包对数据进行统计学处理。 结果: 转染Bmi1 siRNA使SP细胞中Bmi1表达水平下调后,SP细胞的迁移和侵袭能力显著下降;球囊形成率和克隆形成率也显著低于对照组;增殖能力受到抑制;SOD2、Slug和干细胞标志物ABCG2和Nanog的表达水平显著下降。 结论: 沉默Bmi1可调控舌鳞癌侧群细胞的迁移、侵袭和增殖。 相似文献
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多梳蛋白(PcG)家族是非常保守的表观遗传调节因子。近年来对其成员的功能研究发现,PcG家族对干细胞的自我更新及增殖与分化都有很重要的作用。哺乳动物PRC1成员Bmi1和NSPc1在神经系统发育早期高表达。最近的研究提示它们不仅在细胞增殖分化相关基因转录调控中发挥重要作用,而且在神经干细胞自我更新及分化过程中同样有重要作用。 相似文献
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目的 探讨B细胞特异的莫洛尼病毒插入位点1(Bmi1)基因在内皮细胞促进胶质瘤细胞干性表型中的可能作用.方法 以小鼠胶质瘤细胞系GL261和小鼠脑内皮细胞系b.END3为材料,采用Transwell双室细胞共培养、极限稀释法成球实验、实时定量PCR、Western印迹、流式细胞术、体内移植瘤实验以及siRNA基因干扰等方法,检测内皮细胞对胶质瘤细胞体外成球能力和体内成瘤能力、CD133阳性细胞比例、Bmi1基因表达的影响以及抑制Bmi1基因表达对上述现象的影响.结果 与胶质瘤细胞单独培养的对照组相比:(1)胶质瘤细胞与内皮细胞共培养后其体外成球能力明显增强,形成干细胞球数目明显增多(40个细胞/孔的浓度时为62.5%±1.5%比25.0%±4.6%,P=0.000),体积明显增大;内皮细胞与胶质瘤细胞共同移植后所形成的移植瘤出现早、体积更大[(0.798±0.297)比(0.362±0.123) cm3,P=0.000].(2)胶质瘤细胞与内皮细胞共培养后其CD133阳性细胞群比例增大(8.48%±0.78%比4.81%±0.37%,P=0.000).(3)胶质瘤细胞与内皮细胞共培养后Bmi1基因的mRNA(2.72±0.18比1.00±0.15,P=0.000)和蛋白表达明显增加.(4)利用siRNA干扰胶质瘤细胞Bmi1基因表达后,内皮细胞促进胶质瘤细胞干性表型的上述作用明显减弱,敲低Bmi1基因的GL261细胞共培养的CD133阳性比例显著低于共培养的普通GL261细胞(0.34%±0.21%比1.70% ±0.69%,P=0.025).结论 内皮细胞可能通过上调胶质瘤细胞Bmi1基因表达促进胶质瘤细胞的干性表型. 相似文献
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Bmi1 is a polycomb group (Pc-G) protein involved in heritable gene repression, maintenance of cell identity, and proliferation. During the development of the central nervous system, Bmi1 is crucial for self-renewal of neural stem cells and for proliferation of neuronal (granule cell) progenitors of the cerebellum. Here, we use loss of function mouse models and in vitro assays--granule cell cultures and glial-neuronal co-cultures--to show that Bmi1 plays a crucial role in specification of glial progenitors during postnatal cerebellar development. Moreover, we demonstrate in in vitro assays that Bmi1 exerts this novel function through repression of BMP pathway and that this is independent of its known role in mediating the cellular response to Shh signaling. Thus modulation of Bmi1 expression in glial progenitors may represent a key event in determining the differentiation potential of these cells. 相似文献
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Head and neck cancer stem cells: the side population 总被引:1,自引:0,他引:1
Tabor MH Clay MR Owen JH Bradford CR Carey TE Wolf GT Prince ME 《The Laryngoscope》2011,121(3):527-533