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Protease-activated receptor-1 (PAR1) promotes epithelial-endothelial transition through Twist1 in hepatocellular carcinoma

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, August 2018
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Title
Protease-activated receptor-1 (PAR1) promotes epithelial-endothelial transition through Twist1 in hepatocellular carcinoma
Published in
Journal of Experimental & Clinical Cancer Research, August 2018
DOI 10.1186/s13046-018-0858-4
Pubmed ID
Authors

Ting Xiao, Qiang Zhang, Shumin Zong, Wei-long Zhong, Yuan Qin, Zhun Bi, Shuang Chen, Hui-juan Liu, Jun-jie Wei, Bi-jiao Zhou, Lu-meng Wang, Hong-gang Zhou, Yan-rong Liu, Tao Sun, Cheng Yang

Abstract

Tumor cells transfer into endothelial cells by epithelial-endothelial transition (EET), which is characterized by vasculagenic mimicry (VM) in morphology. VM can change tumor microcirculation, progression, and metastasis. However, the molecular mechanisms of endothelial-like transition remain unclear. EET is a subtype of epithelial-mesenchymal transition (EMT). Twist1, a transcriptional regulatory factor of EMT, is an important factor that induces EET in hepatocellular carcinoma(HCC), but the upstream signal of Twist1 is unclear. Expression plasmids, Ca mobilization, and three-dimensional cultures were evaluated. Western blot assay, reporter gene assay, and immunofluorescence staining were conducted. A murine xenograft model was established. Analyses of immunohistochemistry, patient samples, and complementary DNA (cDNA) microarrays were also performed. This study demonstrated that protease-activated receptor-1 (PAR1) can increase the expression of endothelial markers and enhance VM formation by upregulating Twist1 both in vitro and in vivo through thrombin binding. Thrombin not only activates PAR1 but also promotes PAR1 internalization in a time-dependent manner. Clinical pathological analysis further confirms that PAR1 expression is directly correlated with the endothelial marker expression, VM formation, and metastasis and indicates poor survival rate of patients with tumors. PAR1 promotes EET through Twist1 in HCC.

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Mendeley readers

Mendeley readers

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Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 15%
Other 2 10%
Student > Master 2 10%
Student > Postgraduate 2 10%
Researcher 2 10%
Other 1 5%
Unknown 8 40%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 20%
Agricultural and Biological Sciences 3 15%
Medicine and Dentistry 3 15%
Social Sciences 1 5%
Neuroscience 1 5%
Other 0 0%
Unknown 8 40%
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 27 March 2019.
All research outputs
#22,767,715
of 25,385,509 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#1,970
of 2,382 outputs
Outputs of similar age
#298,067
of 340,721 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#66
of 81 outputs
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So far Altmetric has tracked 2,382 research outputs from this source. They receive a mean Attention Score of 4.8. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 81 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.