| Literature DB >> 27389544 |
Yanping Wei1, Qianqian Sun2, Lindong Zhao1, Jianbo Wu2, Xiaonan Chen2, Yuanyuan Wang2, Wenqiao Zang2, Guoqiang Zhao3,4.
Abstract
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.Entities:
Keywords: FOXM1; LncRNA UCA1; Melanoma; miR-507
Mesh:
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Year: 2016 PMID: 27389544 DOI: 10.1007/s12032-016-0804-2
Source DB: PubMed Journal: Med Oncol ISSN: 1357-0560 Impact factor: 3.064