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首页> 外文期刊>Journal of Cellular Physiology >TRAIL up-regulation must be accompanied by a reciprocal PKCepsilon down-regulation during differentiation of colonic epithelial cell: implications for colorectal cancer cell differentiation.
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TRAIL up-regulation must be accompanied by a reciprocal PKCepsilon down-regulation during differentiation of colonic epithelial cell: implications for colorectal cancer cell differentiation.

机译：必须伴随着小道老年病互惠PKCepsilon下调时结肠上皮细胞的分化:对结直肠癌细胞的影响分化。

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摘要

PKC isoenzymes play central roles in various cellular signalling pathways, participating in a variety of protein phosphorylation cascades that regulate/modulate cellular structure and gene expression. It has been firmly established that several isoforms of PKC have a role in the regulation of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) activity. Our interest in probing the role of the epsilon isoform of PKC in the colonic cell differentiation stems from the discovery that PKCepsilon and TRAIL are involved in the differentiation of other cell types like hematopoietic stem cells. Although the role of PKCepsilon and TRAIL in the gastrointestinal system is unclear, it has been observed that PKCepsilon has oncogenic activity in colon epithelial cells (CEC), while TRAIL increases the death of intestinal epithelial cells during inflammation. Here we demonstrate a reciprocal expression of PKCepsilon and TRAIL in human colon mucosa: CECs at the bottom of the colonic crypts show high levels of PKCepsilon, being negative for TRAIL expression. On the contrary, luminal CECs are positive for TRAIL, while negative for PKCepsilon. Indeed, TRAIL- and butyrate-induced differentiation of the human colorectal cancer cell line HT29 requires the decrease of PKCepsilon expression, whose absence in turn increases cell sensitivity to TRAIL-induced apoptosis. Moreover, TRAIL preferentially promotes HT29 differentiation into goblet cells. Taken together, this data demonstrate that TRAIL and PKCepsilon must be reciprocally regulated to ensure physiological CEC differentiation starting from the stem cell pool, and that the down-regulation of PKCepsilon is however critical for the differentiation and apoptosis of cancer cells.
机译：PKC同功酶在各种中发挥核心作用的细胞信号通路参与各种蛋白质的磷酸化途径调节/调节细胞结构和基因表达式。几个亚型的PKC的作用肿瘤坏死factor-related监管细胞凋亡诱导配体(TRAIL)活动。探索ε的角色的兴趣同种型结肠细胞PKC分化源于发现PKCepsilon和小道是参与分化的细胞类型造血干细胞。PKCepsilon和胃肠道的小道系统尚不清楚,它已被观察到PKCepsilon在结肠致癌活性上皮细胞(CEC),而增加了中肠上皮细胞的死亡炎症。在人类结肠PKCepsilon表达式和小径粘膜:个cec上结肠隐窝的底部展示高水平的PKCepsilon,是负面的的轨迹表达式。cec阳性,而为阴性PKCepsilon。分化的人类结肠直肠癌细胞系HT29需要的减少PKCepsilon表达的缺失增加细胞TRAIL-induced敏感性细胞凋亡。促进HT29细胞分化成杯状细胞。综上所述,这些数据证明和PKCepsilon必须相互地监管确保生理CEC分化开始从干细胞池,下调PKCepsilon不过是至关重要的分化和凋亡的癌症细胞。

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