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MicroRNA-328 enhances cellular motility through posttranscriptional regulation of PTPRJ in human hepatocellular carcinoma

Overview of attention for article published in OncoTargets and therapy, October 2015
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Title
MicroRNA-328 enhances cellular motility through posttranscriptional regulation of PTPRJ in human hepatocellular carcinoma
Published in
OncoTargets and therapy, October 2015
DOI 10.2147/ott.s93056
Pubmed ID
Authors

Xiaoling Luo, Shiyan Yang, Chuanwen Zhou, Feng Pan, Qianjun Li, Shijie Ma

Abstract

Interaction between microRNA (miR-328) and PTPRJ (protein tyrosine phosphatase, receptor type, J) has been reported to be responsible for miR-328-dependent increase in epithelial cancer cell proliferation. However, the role of miR-328 and PTPRJ in hepatocellular carcinoma (HCC) remains unclear. The aim of this study was to investigate the clinical significance of miR-328 and/or PTPRJ expression in human HCC and determine their precise biological functions in this malignancy. Expression levels of miR-328 and PTPRJ messenger RNA (mRNA) in 100 pairs of HCC and adjacent noncancerous tissues were detected using quantitative real-time reverse transcription polymerase chain reaction. The associations between miR-328 and/or PTPRJ expression and various clinicopathological features of HCC patients were further statistically assessed. Then, the functions of miR-328 and PTPRJ in migration and invasion of two human HCC cell lines were determined by transwell assays. miR-328 and PTPRJ mRNA expression levels were markedly upregulated and down-regulated in HCC tissues, respectively, compared to adjacent noncancerous tissues. Notably, the upregulation of miR-328 in HCC tissues was significantly correlated with the downregulation of PTPRJ mRNA in HCC tissues (r=-0.362, P=0.01). In addition, miR-328-high and/or PTPRJ-low expression were found to be closely correlated with high Edmondson-Steiner grading (all P<0.05) and advanced tumor-node-metastasis stage (all P<0.05). Moreover, the restoration of miR-328 dramatically promoted HCC cell migration and invasion by repressing PTPRJ expression. Interestingly, the loss of PTPRJ expression could significantly attenuate the inhibitory effects of knockdown miR-328 on the migration and invasion of HCC cells. These findings demonstrated that the dysregulation of miR-328 and PTPRJ may be associated with tumor progression of HCC patients. Functionally, miR-328 may serve as a crucial oncogene and be implicated in the motility of HCC cells at least in part by the suppression of PTPRJ.

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Mendeley readers

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Geographical breakdown

Country Count As %
Unknown 10 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 30%
Other 1 10%
Student > Bachelor 1 10%
Lecturer 1 10%
Student > Master 1 10%
Other 1 10%
Unknown 2 20%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 60%
Medicine and Dentistry 2 20%
Unknown 2 20%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 November 2015.
All research outputs
#22,759,452
of 25,373,627 outputs
Outputs from OncoTargets and therapy
#2,078
of 3,016 outputs
Outputs of similar age
#245,757
of 286,876 outputs
Outputs of similar age from OncoTargets and therapy
#65
of 105 outputs
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We're also able to compare this research output to 105 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.