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MiR-875-5p inhibits hepatocellular carcinoma cell proliferation and migration by repressing astrocyte elevated gene-1 (AEG-1) expression

  
@article{TCR18950,
	author = {Caixia Hu and Shichang Cui and Jiasheng Zheng and Tian Yin and Junsheng Lv and Jiang Long and Wenwen Zhang and Xun Wang and Shoupeng Sheng and Honghai Zhang and Yu Sun and Hongguang Wang and Cong Li},
	title = {MiR-875-5p inhibits hepatocellular carcinoma cell proliferation and migration by repressing astrocyte elevated gene-1 (AEG-1) expression},
	journal = {Translational Cancer Research},
	volume = {7},
	number = {1},
	year = {2018},
	keywords = {},
	abstract = {Background: Liver cancer or hepatocellular carcinoma (HCC) is one of the prevalent cancers with high mortality rate. There is no effective treatment for patients with unresectable HCC and approach for preventing metastasis. 
Methods: The expression of miR-875-5p in HCC clinical samples was quantified by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of miR-875-5p or astrocyte elevated gene-1 (AEG-1) on cancer cell migration and invasion were performed by transwell assay. The cell cycle analysis was performed by FACS. Luciferase- reporter assay showed that miR-875-5p targets the 3'-untranslated region (3'-UTR) of AEG-1 to negatively regulate AEG-1 expression. 
Results: In this study, we found miR-875-5p, a potential tumor suppressing miRNA reported recently, was significantly decreased in HCC tissues. Overexpression of miR-875-5p inhibited cell migration, invasion, EMT progression and angiogenesis. In addition, miR-875-5p regulated AEG-1 by directly binding to its 3’-UTR. In clinical samples of HCC, miR-875-5p was inversely correlated with AEG-1, which was upregulated in HCC. Deficiency of AEG-1 expression partially suppressed the migration, invasion, EMT progression and angiogenesis in MHCC97-H cell line. 
Conclusions: Taken together, these results elucidate the functions of miR-875-5p and its targets AEG-1 in HCC, not only broadening our understanding of them in HCC development, but also suggesting their therapeutic potential in HCC treatment.},
	issn = {2219-6803},	url = {https://tcr.amegroups.org/article/view/18950}
}