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miR-200b/c-RAP1B axis represses tumorigenesis and malignant progression of papillary thyroid carcinoma through inhibiting the NF-κB/Twist1 pathway.
Experimental Cell Research ( IF 3.7 ) Pub Date : 2019-12-23 , DOI: 10.1016/j.yexcr.2019.111785
Bo Zhou 1 , Jing Xu 2 , Ye Chen 3 , Shegan Gao 3 , Xiaoshan Feng 3 , Xiubo Lu 4
Affiliation  

Papillary thyroid carcinoma (PTC) is a common endocrine malignancy with an increasing occurrence and recurrence. MicroRNAs (miRNAs) have been widely acknowledged to be participated in human cancers. However, how these miRNAs exert roles and potential mechanisms in PTC regulatory networks is still lacking. The purpose of our study lies in discovering the regulatory basis of miR-200b/c and Rap1b for PTC tumorigenesis and malignant progression, as well as the underlying molecular mechanisms. Herein, miR-200b/c expression was sharply dropped and Rap1b expression was up-regulated in PTC cells and tissues samples when compared to normal thyroid epithelial cells and normal tissues. miR-200b/c targeted Rap1 directly and negatively regulated its expression. miR-200b/c overexpression suppressed proliferative, colony forming, migratory and invasive capabilities and EMT as well as elevated apoptosis of PTC cells through inhibiting Rap1b. Furthermore, xenograft experiments showed miR-200b/c overexpression constrained growth of PTC xenograft and EMT. miR-200b/c inhibited NF-κB/Twist1 signals via regulating the Rap1b expression in cells and animal models. Taken together, our study suggested that upregulation of miR-200b/c-RAP1B axis constrained PTC cell proliferation, invasion, migration and EMT. Also, the upregulation of miR-200b/c-RAP1B leaded to elevated apoptosis through inhibiting the NF-κB/Twist1 pathway, thus inhibiting PTC tumorigenesis and malignant progression.

中文翻译:

miR-200b / c-RAP1B轴通过抑制NF-κB/ Twist1途径抑制甲状腺乳头状癌的发生和恶性进展。

甲状腺乳头状癌(PTC)是一种常见的内分泌恶性肿瘤,其发生率和复发率均在增加。MicroRNA(miRNA)已被广泛认为参与人类癌症。但是,仍然缺少这些miRNA如何在PTC调节网络中发挥作用和潜在机制。我们研究的目的在于发现miR-200b / c和Rap1b对PTC肿瘤发生和恶性进展的调控基础,以及潜在的分子机制。在此,与正常甲状腺上皮细胞和正常组织相比,在PTC细胞和组织样品中miR-200b / c表达急剧下降,Rap1b表达上调。miR-200b / c直接靶向Rap1,并对其表达负调控。miR-200b / c过表达抑制增殖,集落形成,迁移和侵袭能力,EMT以及通过抑制Rap1b导致PTC细胞凋亡增加。此外,异种移植物实验显示miR-200b / c过表达限制了PTC异种移植物和EMT的生长。miR-200b / c通过调节细胞和动物模型中Rap1b的表达抑制NF-κB/ Twist1信号。综上所述,我们的研究表明miR-200b / c-RAP1B轴的上调抑制了PTC细胞的增殖,侵袭,迁移和EMT。而且,miR-200b / c-RAP1B的上调通过抑制NF-κB/ Twist1途径导致凋亡增加,从而抑制PTC的肿瘤发生和恶性进展。miR-200b / c通过调节细胞和动物模型中Rap1b的表达抑制NF-κB/ Twist1信号。综上所述,我们的研究表明miR-200b / c-RAP1B轴的上调抑制了PTC细胞的增殖,侵袭,迁移和EMT。而且,miR-200b / c-RAP1B的上调通过抑制NF-κB/ Twist1途径导致凋亡增加,从而抑制PTC的肿瘤发生和恶性进展。miR-200b / c通过调节细胞和动物模型中Rap1b的表达抑制NF-κB/ Twist1信号。综上所述,我们的研究表明miR-200b / c-RAP1B轴的上调抑制了PTC细胞的增殖,侵袭,迁移和EMT。而且,miR-200b / c-RAP1B的上调通过抑制NF-κB/ Twist1途径导致凋亡增加,从而抑制PTC的肿瘤发生和恶性进展。
更新日期:2019-12-23
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