Pituitary tumor-transforming gene 1 enhances metastases of cervical cancer cells through miR-3666-regulated ZEB1

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• 作者：Lin Li ; Li-Ying Han ; Ming Yu ; Qi Zhou ; Jian-Cheng Xu ; Ping Li
• 关键词：Cervical cancer (CC) ; ZEB1 ; miR ; 3666 ; Pttg1
• 刊名：Tumor Biology
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：37
• 期：12
• 页码：15567-15573
• 全文大小：
• 刊物主题：Cancer Research;
• 出版者：Springer Netherlands
• ISSN：1423-0380
• 卷排序：37

文摘

Early cancer metastases often occur in cervical cancer (CC) patients, resulting in poor prognosis and poor therapeutic outcome after resection of primary cancer. Hence, there is a compelling requirement for elucidating the molecular mechanisms underlying the CC cell invasiveness. Recently, the role of microRNAs (miRNAs) and pituitary tumor-transforming gene 1 (Pttg1) in the carcinogenesis of CC has been reported. Nevertheless, the relationship between miRNAs and Pttg1 remains ill-defined. Here, we showed that the levels of miR-3666 were significantly decreased and the levels of zinc finger E-box binding homeobox 1 (ZEB1) and Pttg1 were significantly increased in the CC specimens from patients, compared to the paired non-tumor tissue. Moreover, the levels of miR-3666 and ZEB1 inversely correlated. Bioinformatics analyses showed that miR-3666 targeted the 3′-untranslated region (3′-UTR) of ZEB1 messenger RNA (mRNA) to inhibit its translation, which was confirmed by luciferase reporter assay. Moreover, Pttg1 overexpression inhibited miR-3666 and subsequently increased ZEB1 and cell invasion, while Pttg1 depletion increased miR-3666 and subsequently decreased ZEB1 and cell invasion. Together, our data suggest that Pttg1 may increase CC cell metastasis, possibly through miR-3666-regulated ZEB1 levels.