LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma
LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma
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DOI：
10.1007/s12032-016-0804-2
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发表时间：
2016-08-01
期刊：
影响因子：
3.4
通讯作者：
Zhao, Guoqiang
中科院分区：
文献类型：
--
作者：
Wei, Yanping;Sun, Qianqian;Zhao, Guoqiang
最近，黑色素瘤的发病率一直在上升。有远处转移者预后差。越来越多的研究已经进行，以澄清的分子机制，以及探讨潜在的有效的治疗靶点在黑色素瘤的发展。本研究对LncRNA UCA1及其下游调控因子进行了研究。在我们的实验中，发现UCA 1在黑色素瘤组织和细胞中表达上调，而UCA 1的缺失导致细胞增殖、侵袭和细胞周期停滞的抑制。为了进一步了解UCA 1的作用机制，我们建立了一个实验系统。我们发现miR-507可以在miRNA识别位点直接与UCA1结合，并且miR-507与UCA1之间存在负相关性。此外，FOXM1是miR-507的靶点，并且可以通过miR-507过表达或UCA 1耗尽而下调。下调FOXM1类似于UCA1的耗竭和miR-507的过表达。这些结果，综合起来，提供了一个新的UCA1相互作用的黑色素瘤的肿瘤发生调控网络的证据。
Recently, the incidence of melanoma has been on the rise. Patients with distant metastasis share poor prognosis. Increasing studies have been conducted to clarify the molecular mechanisms as well as to investigate potential effective therapeutic targets in the development of melanoma. This study focuses on the LncRNA UCA1 and its downstream regulated factors. In our experiments, UCA1 expression was discovered to be upregulated in melanoma tissues and cells, while the depletion of UCA1 led to the inhibition of cell proliferation, invasion and cell cycle arrest. To further our understanding of the mechanisms of UCA1, a system of experiments was built. We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507. These results, taken together, provide evidence for a novel UCA1 interaction regulatory network in tumorigenesis of melanoma.