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SGK1 inhibition-induced autophagy impairs prostate cancer metastasis by reversing EMT

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, April 2018
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Title
SGK1 inhibition-induced autophagy impairs prostate cancer metastasis by reversing EMT
Published in
Journal of Experimental & Clinical Cancer Research, April 2018
DOI 10.1186/s13046-018-0743-1
Pubmed ID
Authors

Weiwei Liu, Xuchu Wang, Yiyun Wang, Yibei Dai, Yiyi Xie, Ying Ping, Binbin Yin, Pan Yu, Zhenping Liu, Xiuzhi Duan, Zhaoping Liao, Yuhua Chen, Chunhua Liu, Xiang Li, Zhihua Tao

Abstract

Despite SGK1 has been identified and characterized as a tumor-promoting gene, the functions and underlying mechanisms of SGK1 involved in metastasis regulation have not yet been investigated in cancer. We investigated the cellular responses to GSK650394 treatment and SGK1 silencing (or overexpression) in human prostate cancer (PCa) cell lines and PC3 xenografts by wound healing assay, migration and invasion assay, western blotting, immunofluorescence and immunohistochemistry. In the present study, we found that SGK1 expression positively correlates with human prostate cancer (PCa) progression and metastasis. We show that SGK1 inhibition significantly attenuates EMT and metastasis both in vitro and in vivo, whereas overexpression of SGK1 dramaticlly promoted the invasion and migration of PCa cells. Our further results suggest that SGK1 inhibition induced antimetastatic effects, at least partially via autophagy-mediated repression of EMT through the downregulation of Snail. Moreover, ectopic expression of SGK1 obviously attenuated the GSK650394-induced autophagy and antimetastatic effects. What's more, dual inhibition of mTOR and SGK1 enhances autophagy and leads to synergistic antimetastatic effects on PCa cells. Taken together, this study unveils a novel mechanism in which SGK1 functions as a tumor metastasis-promoting gene and highlights how co-targeting SGK1 and autophagy restrains cancer progression due to the amplified antimetastatic effects.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 42 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 6 14%
Student > Master 4 10%
Student > Ph. D. Student 4 10%
Student > Bachelor 4 10%
Student > Doctoral Student 3 7%
Other 8 19%
Unknown 13 31%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 11 26%
Medicine and Dentistry 6 14%
Pharmacology, Toxicology and Pharmaceutical Science 2 5%
Chemistry 2 5%
Unspecified 1 2%
Other 5 12%
Unknown 15 36%
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 08 April 2018.
All research outputs
#19,951,180
of 25,382,440 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#1,462
of 2,380 outputs
Outputs of similar age
#251,818
of 342,742 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#25
of 39 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,380 research outputs from this source. They receive a mean Attention Score of 4.8. This one is in the 31st percentile – i.e., 31% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 342,742 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 21st percentile – i.e., 21% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 39 others from the same source and published within six weeks on either side of this one. This one is in the 30th percentile – i.e., 30% of its contemporaries scored the same or lower than it.