期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1865, 期 10, 页码 1479-1490出版社
ELSEVIER
DOI: 10.1016/j.bbamcr.2018.07.008
关键词
Long non-coding RNA plasmacytoma variant translocation 1 (PVT1); miR-195-5p; Acidic fibroblast growth factor receptor (FGFR1); Basic fibroblast growth factor (FGF2); Endometrial carcinoma
资金
- National Natural Science Foundation of China [81272874, 81472438]
- Department of Science and Technology of Liaoning Province [2013225079]
- Shenyang City Science and Technology Bureau [F14-158-9-47]
- Outstanding Scientific Fund of Shengjing Hospital [201601]
- Shengjing Hospital excellent subject [ME40]
- [2014-187]
The plasmacytoma variant translocation 1 (PVT1) 1 gene is a long non-coding RNA (IncRNA) 2 that has been shown to be an oncogene in many cancers. Herein, the function and potential molecular mechanisms connecting PVT1 and miR-195-5p were elucidated in endometrial cancer cell lines. Quantitative real-time PCR and fluorescence in situ hybridization (FISH) 3 demonstrated that PVT1 is up-regulated concomitant with miR-195-5p down-regulation in human endometrial carcinoma tissues. PVT1 knockdown inhibited cell proliferation, migration, and invasion while facilitating apoptosis of endometrial cancer cells. Moreover, restoration of miR-1955p due to PVT1 knockdown exerted tumor-suppressive functions. We observed that PVT1 promotes malignant cell behavior by decreasing miR-195-5p expression. Binding of PVT1 and miR-195-5p was confirmed using luciferase assays. Furthermore, expression of miR-195-5p negatively correlates with PVT1 expression. At the molecular level, either PVT1 knockdown or miR-195-5p overexpression resulted in a decrease of acidic fibroblast growth factor receptor (FGFR1) 4 and basic fibroblast growth factor (FGF2). 5 FGFR1 and FGF2 are targets of miR195-5p that play a critical role in endometrial carcinoma by activating PI3K/AKT and MAPK/Erk pathways. Remarkably, PVT1 knockdown combined with miR-195-5p overexpression led to tumor regression in vivo. Overall, these results depict a novel pathway mediated by PVT1 in endometrial carcinoma, which may have potential application for endometrial carcinoma therapy.
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