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首页> 外文期刊>Journal of cellular physiology. >microRNA-377 acts as a suppressor in esophageal squamous cell carcinoma through CBX3-dependent P53/P21 pathway
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microRNA-377 acts as a suppressor in esophageal squamous cell carcinoma through CBX3-dependent P53/P21 pathway

机译：microrna在食管- 377作为抑制通过CBX3-dependent鳞状细胞癌P53、P21通路

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摘要

Stem cells play pivotal roles in esophageal squamous cell carcinoma (ESCC) recurrence and metastasis. The self-renewal ability of stem cells was associated with specific microRNAs (miRs). Herein, we identified the effects of miR-377 on ESCC stem cell activities. First, the expression of miR-377 in ESCC and adjacent normal tissues was determined. The relationship between miR-377 and chromobox protein homolog 3 (CBX3) was assessed by a dual-luciferase reporter gene assay. miR-377 was overexpressed or inhibited in ESCC stem cells to explore its role in ESCC. To further investigate the mechanism of miR-377 in ESCC, cells were introduced with short hairpin RNA against CBX3 or pifithrin-alpha (inhibitor of P53 pathway). Besides, the expression of P21, P53, CD133, CD13, Nanog, sex determining region Y-Box 2 (Sox2), and octamer-binding transcription factor 4 (Oct4), cell sphere formation, colony formation, and proliferation were evaluated respectively. Finally, limiting dilution assay in vivo and tumor xenograft in nude mice were conducted to confirm the roles of miR-377 in vivo. miR-377 was poorly expressed in ESCC. Overexpression of miR-377 could suppress the stem-like trait of ESCC as well as the tumor growth in vivo. miR-377 targeted CBX3 to activate the P53/P21 pathway. Besides, the expression of stem-like markers including CD133, CD13, Oct4, Sox2, and Nanog was decreased, and the abilities of cell sphere formation, colony formation, proliferation, and tumorigenicity were significantly reduced by overexpressing miR-377 or silencing CBX3. The results were reversed after inactivating the P53/P21 pathway. In summary, upregulation of miR-377 inhibits the self-renewal of ESCC stem cells by inhibiting CBX3 expression and promoting activation of the P53/P21 pathway.
机译：干细胞在食管扮演关键的角色鳞状细胞癌(ESCC)复发转移。细胞是与特定的小分子核糖核酸相关联(大鹏)。mir - 377对ESCC干细胞活动。mir - 377的表达在ESCC和相邻的正常组织决定。mir - 377和chromobox同族体蛋白3 (CBX3)是由一个dual-luciferase评估报告基因化验。在ESCC ESCC干细胞,探讨它的作用。进一步调查mir - 377的机制ESCC,介绍了细胞短发夹RNA对CBX3或pifithrin-alpha(抑制剂P53通路)。P53、CD133 CD13、Nanog、性别确定区域Y-Box 2 (Sox2), octamer-binding转录因子4 (Oct4)、细胞球体形成、殖民地形成和扩散进行了评估分别。在裸小鼠体内和肿瘤异种移植进行确认mir - 377的角色vivo超表达mir - 377可能抑制ESCC以及肿瘤干细胞的特征增长的体内。P53、P21途径。干细胞标志物CD133、CD13、Oct4、Sox2, Nanog是减少,和能力集落形成细胞球的形成,扩散,致瘤性大大减少了overexpressing mir - 377或沉默CBX3。灭活后P53、P21通路。总结,upregulation mir - 377抑制了抑制ESCC干细胞的自我更新CBX3表达式和促进的激活P53、P21途径。

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