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Identification of endonuclease domain-containing 1 as a novel tumor suppressor in prostate cancer

Overview of attention for article published in BMC Cancer, May 2017
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Title
Identification of endonuclease domain-containing 1 as a novel tumor suppressor in prostate cancer
Published in
BMC Cancer, May 2017
DOI 10.1186/s12885-017-3330-5
Pubmed ID
Authors

Jianguang Qiu, Shubin Peng, Jie Si-Tu, Cheng Hu, Wentao Huang, Yunhua Mao, Wenhan Qiu, Ke Li, Dejuan Wang

Abstract

Endonuclease domain containing 1 (ENDOD1) is implicated in tumorigenesis and aggressiveness of multiple tumors. In this study, we aimed to investigate the role of ENDOD1 in prostate cancer (PCa). Immunohistochemistry were performed in 30 cases of benign prostatic hyperplasia (BPH) and 50 cases of PCa to identify its association with clinicopathological characteristics. Real-time PCR and western blot were used to detect ENDOD1 mRNA and protein expression in normal prostatic epithelial and PCa cell lines. MTT assays were employed to determine the effect of cell proliferation. Flow cytometry was used to explore the cell cycle distribution and apoptotic effects. Transwell migration and invasion assays were done to evaluate changes in the ability of cell migration and invasion. Immunoreactivity scores of ENDOD1 showed no statistical difference between BPH and low-grade PCa, whereas lower immunostaining scores were observed in high-grade compared with low-grade PCa. Real-time PCR data indicated that ENDOD1 mRNA expression was markedly increased in LNCaP and 22Rv1 cells and decreased in PC3 and DU145 cells compared to the normal epithelial cells RWPE1. Western blot showed that androgen-sensitive LNCaP cells had the highest protein expression level of ENDOD1, whereas castration-resistant PCa cell lines PC3 and DU145 had significantly lower protein levels. Meanwhile, overexpression of ENDOD1 suppressed cell proliferation, induced G0/G1 cell cycle arrest and inhibited cell migration and invasion. Conversely, siRNA-mediated silencing of ENDOD1 promoted cell proliferation, migration and invasion. No apoptotic effects occurred upon manipulation of ENDOD1 expression. Our results indicate that ENDOD1 is a novel tumor suppressor in PCa, which may be employed as a new drug target of preventing progression to metastatic castration-resistant prostate cancer.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 18 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 22%
Student > Master 3 17%
Student > Bachelor 3 17%
Librarian 1 6%
Other 1 6%
Other 2 11%
Unknown 4 22%
Readers by discipline Count As %
Social Sciences 2 11%
Veterinary Science and Veterinary Medicine 1 6%
Biochemistry, Genetics and Molecular Biology 1 6%
Nursing and Health Professions 1 6%
Agricultural and Biological Sciences 1 6%
Other 5 28%
Unknown 7 39%
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 28 May 2017.
All research outputs
#20,425,762
of 22,977,819 outputs
Outputs from BMC Cancer
#6,523
of 8,348 outputs
Outputs of similar age
#273,042
of 313,717 outputs
Outputs of similar age from BMC Cancer
#112
of 142 outputs
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So far Altmetric has tracked 8,348 research outputs from this source. They receive a mean Attention Score of 4.3. 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 142 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.