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RIF1 promotes human epithelial ovarian cancer growth and progression via activating human telomerase reverse transcriptase expression

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, August 2018
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Title
RIF1 promotes human epithelial ovarian cancer growth and progression via activating human telomerase reverse transcriptase expression
Published in
Journal of Experimental & Clinical Cancer Research, August 2018
DOI 10.1186/s13046-018-0854-8
Pubmed ID
Authors

Yong-Bin Liu, Ying Mei, Jing Long, Yu Zhang, Dong-Li Hu, Hong-Hao Zhou

Abstract

Human telomerase reverse transcriptase (hTERT) is highly expressed in over 80% of tumors, including human epithelial ovarian cancer (EOC). However, the mechanisms through which hTERT is up-regulated in EOC and promotes tumor progression remain unclear. The aim of this study is to identify RIF1 as a novel molecular target that modulate hTERT signaling and EOC growth. RIF1 expression in ovarian cancer, benign and normal ovarian tissues was examined by immunohistochemistry. The biological role of RIF1 was revealed by MTS, colony formation and sphere formation assays. Luciferase reporter assay and chromatin immunoprecipitation (CHIP) assay were used to verify RIF1 as a novel hTERT promoter-binding protein in EOC cells. The role of RIF1 on tumorigenesis in vivo was detected by the xenograft model. RIF1 expression is upregulated in EOC tissues and is closely correlated with FIGO stage and prognosis of EOC patients. Functionally, RIF1 knockdown suppressed the expression and promoter activity of hTERT and consequently inhibited the growth and CSC-like traits of EOC cells. RIF1 knockdown also inhibited tumorigenesis in xenograft model. RIF1 overexpression had the opposite effect. Luciferase reporter assay and ChIP assay verified RIF1 directly bound to hTERT promoter to upregulate its expression. The rescue experiments suggested hTERT overexpression rescued the inhibition of EOC cell growth and CSC-like traits mediated by RIF1 knockdown. Consistently, hTERT knockdown abrogated the RIF1-induced promotion of EOC cell growth and CSC-like traits. RIF1 promotes EOC progression by activating hTERT and the RIF1/hTERT pathway may be a potential therapeutic target for EOC patients.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 15 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 15 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 27%
Librarian 1 7%
Other 1 7%
Professor 1 7%
Student > Bachelor 1 7%
Other 2 13%
Unknown 5 33%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 27%
Pharmacology, Toxicology and Pharmaceutical Science 2 13%
Medicine and Dentistry 2 13%
Social Sciences 1 7%
Agricultural and Biological Sciences 1 7%
Other 0 0%
Unknown 5 33%
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 05 August 2018.
All research outputs
#20,663,600
of 25,385,509 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#1,636
of 2,382 outputs
Outputs of similar age
#265,205
of 341,622 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#49
of 80 outputs
Altmetric has tracked 25,385,509 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
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 17th percentile – i.e., 17% 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 341,622 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 12th percentile – i.e., 12% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 80 others from the same source and published within six weeks on either side of this one. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.