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Kindlin-2 promotes hepatocellular carcinoma invasion and metastasis by increasing Wnt/β-catenin signaling

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, September 2017
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Title
Kindlin-2 promotes hepatocellular carcinoma invasion and metastasis by increasing Wnt/β-catenin signaling
Published in
Journal of Experimental & Clinical Cancer Research, September 2017
DOI 10.1186/s13046-017-0603-4
Pubmed ID
Authors

Jie Lin, Wansong Lin, Yunbin Ye, Liping Wang, Xiaoyan Chen, Shengbing Zang, Aimin Huang

Abstract

Kindlin-2 is a member of the focal adhesion protein family that regulates invasion and metastasis in multiple malignancies; however, little is known about the role of Kindlin-2 in hepatocellular carcinoma (HCC) progression. Immunohistochemistry was used to investigate Kindlin-2 expression in 177 pairs of human HCC and adjacent liver tissue samples. The role of Kindlin-2 in the in vitro invasion and migration of HCC cell lines was evaluated in MHCC97H, LM3 and SMMC7721 cells. Microarray expression analysis was applied to explore the molecular mechanism through which Kindlin-2 promoted HCC progression. Quantitative real-time PCR and Western blotting were performed to verify the microarray results. High Kindlin-2 expression was found to significantly correlate with aggressive HCC clinicopathological features including tumor encapsulation, microvascular invasion, extrahepatic metastasis and poor prognosis. In vitro, Kindlin-2 knockout or knockdown inhibited HCC cell adhesion, migration and invasion, while ectopic Kindlin-2 expression promoted these processes. Importantly, Kindlin-2 activated Wnt/β-catenin signaling and increased β-catenin expression, especially levels of non-phosphorylated β-catenin, as well as two Wnt/β-catenin signaling pathway targets, Axin2 and MMP7. Kindlin-2 also induced a change in the expression profile of HCC cells, suggesting the cells underwent epithelial-mesenchymal transition. For example, the expression of the epithelial marker E-cadherin was downregulated, while the mesenchymal markers Vimentin, N-cadherin and Snail were upregulated. Kindlin-2 promotes HCC invasion, metastasis and epithelial-mesenchymal transition through Wnt/β-catenin signaling.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 9 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 9 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 3 33%
Student > Postgraduate 1 11%
Unspecified 1 11%
Student > Bachelor 1 11%
Student > Ph. D. Student 1 11%
Other 2 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 44%
Medicine and Dentistry 2 22%
Agricultural and Biological Sciences 1 11%
Social Sciences 1 11%
Unspecified 1 11%
Other 0 0%

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 13 July 2018.
All research outputs
#11,734,749
of 13,218,736 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#672
of 898 outputs
Outputs of similar age
#230,482
of 266,390 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#1
of 1 outputs
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So far Altmetric has tracked 898 research outputs from this source. They receive a mean Attention Score of 2.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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