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Critical role of CDK11p58 in human breast cancer growth and angiogenesis

Overview of attention for article published in BMC Cancer, October 2015
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Title
Critical role of CDK11p58 in human breast cancer growth and angiogenesis
Published in
BMC Cancer, October 2015
DOI 10.1186/s12885-015-1698-7
Pubmed ID
Authors

Yayun Chi, Sheng Huang, Haojie Peng, Mengying Liu, Jun Zhao, Zhiming Shao, Jiong Wu

Abstract

A capillary network is needed in cancer growth and metastasis. Induction of angiogenesis represents one of the major hallmarks of cancer. CDK11(p58), a Ser/Thr kinase that belongs to the Cell Division Cycle 2-like 1 (CDC2L1) subfamily is associated with cell cycle progression, tumorigenesis, sister chromatid cohesion and apoptotic signaling. However, its role in breast cancer proliferation and angiogenesis remains unclear. Tumorigenicity assays and blood vessel assessment in athymic mice were used to assess the function of CDK11(p58) in tumor proliferation and angiogenesis. CCK-8 assay was used to detect breast cancer cell growth. Immunohistochemistry was used to detect the expression of vascular endothelial growth factor (VEGF), CD31 and CD34 in CDK11 positive patient breast cancer tissues. Dual-Luciferase array was used to analyze the function of CDK11(p58) in the regulation of VEGF promoter activity. Western blot was used to detect related protein expression levels. CDK11(p58) inhibited breast cancer growth and angiogenesis in breast cancer cells and in nude mice transplanted with tumors. Immunohistochemistry confirmed that CDK11(p58) was negatively associated with angiogenesis-related proteins such as VEGF, CD31 and CD34 in breast cancer patients. Real-time PCR and dual-luciferase assay showed CDK11(p58) inhibited the mRNA levels of VEGF and the promoter activity of VEGF. As CDK11(p58) is a Ser/Thr kinase, the kinase-dead mutant failed to inhibit VEGF mRNA and promoter activity. Western blot analysis showed the same pattern of related protein expression. The data suggested angiogenesis inhibition was dependent on CDK11(p58) kinase activity. This study indicates that CDK11(p58) inhibits the growth and angiogenesis of breast cancer dependent on its kinase activity.

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X Demographics

The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 18%
Researcher 2 12%
Student > Postgraduate 2 12%
Student > Master 2 12%
Other 1 6%
Other 2 12%
Unknown 5 29%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 35%
Environmental Science 1 6%
Pharmacology, Toxicology and Pharmaceutical Science 1 6%
Agricultural and Biological Sciences 1 6%
Immunology and Microbiology 1 6%
Other 1 6%
Unknown 6 35%
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 17 October 2015.
All research outputs
#18,141,324
of 23,305,591 outputs
Outputs from BMC Cancer
#5,056
of 8,440 outputs
Outputs of similar age
#189,548
of 280,353 outputs
Outputs of similar age from BMC Cancer
#126
of 235 outputs
Altmetric has tracked 23,305,591 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 8,440 research outputs from this source. They receive a mean Attention Score of 4.4. This one is in the 34th percentile – i.e., 34% 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 280,353 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 235 others from the same source and published within six weeks on either side of this one. This one is in the 38th percentile – i.e., 38% of its contemporaries scored the same or lower than it.