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miRNA-451 inhibits proliferation and motility of the gastric cancer SGC-7901 cell line via targeting AKT-mediated signal pathway

  
@article{TCR17412,
	author = {Biao Chen and Jun-Jian Deng and Wei Ge and Yong-Fa Zheng and De-Dong Cao and Ximing Xu},
	title = {miRNA-451 inhibits proliferation and motility of the gastric cancer SGC-7901 cell line via targeting AKT-mediated signal pathway},
	journal = {Translational Cancer Research},
	volume = {6},
	number = {6},
	year = {2017},
	keywords = {},
	abstract = {Background: miRNAs are a group of non-coding RNAs that play an important role in in regulating tumour development and progression. Recently, increased evidences have reported that altered miRNA-451 is implicated in carcinogenesis of various types of human cancer. However, the expression and roles of miRNA-451 in gastric cancer (GC) remain to be established. 
Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay was performed to measure the expression of miRNA-451 in GC tissue samples and cell lines. Then, the effects of miRNA-451 on growth, colony formation, apoptosis, migration and invasion of SGC-7901 cells were focused upon after transient transinfection of miRNA-451 mimics. Finally, the effects of miRNA-451 upregulation on AKTmediated signal pathway were also determined. 
Results: miRNA-451 was found to be significantly down-regulated in gastric cancer tissues and cell lines. In addition, Functional studies indicated that the forced expression of miRNA-451 could suppress cell proliferation, colony formation, cellular migration and invasion of SGC-7901 cells. Moreover, we uncovered that AKT-mediated signal pathway has been partially inactivated at post-transcriptional levels with upregulation of miRNA-451. 
Conclusions: These findings support the role of miRNA-451 as a regulator of GC progression partially via attenuating AKT-mediated signal pathway. Thus, miRNA-451 may become novel promising potential therapeutic targets for gastric cancer.},
	issn = {2219-6803},	url = {https://tcr.amegroups.org/article/view/17412}
}