↓ Skip to main content

S100A16 promotes cell proliferation and metastasis via AKT and ERK cell signaling pathways in human prostate cancer

Overview of attention for article published in Tumor Biology, May 2016
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age and source

Mentioned by

twitter
1 X user

Citations

dimensions_citation
46 Dimensions

Readers on

mendeley
23 Mendeley
Title
S100A16 promotes cell proliferation and metastasis via AKT and ERK cell signaling pathways in human prostate cancer
Published in
Tumor Biology, May 2016
DOI 10.1007/s13277-016-5096-9
Pubmed ID
Authors

Weidong Zhu, Yi Xue, Chao Liang, Rihua Zhang, Zhihong Zhang, Hongyan Li, Dongming Su, Xiubin Liang, Yuanyuan Zhang, Qiong Huang, Menglan Liu, Lu Li, Dong Li, Allan Z. Zhao, Yun Liu

Abstract

S100A16 is a member of the S100 calcium-binding protein family. It is overexpressed in many types of tumors and associated with proliferation, migration, and invasion; however, its function in human prostate cancer is unresolved. Our objective was to determine its effects and the underlying pathways of S100A16 in prostate cancer tissues and cells. We measured S100A16 expression by quantitative real-time polymerase and Western blotting in eight matched prostate cancer and adjacent normal tissues, and in three prostate cancer cell lines, DU-145, LNCaP, and PC-3, compared to a normal prostate epithelial cell line PrEC. DU-145 cells stably overexpressing S100A16 and PC-3 cells with S100A16 knockdown were established by transfection with S100A16 overexpression plasmid or shRNAs. Invasion, migration, and proliferation were analyzed by transwell assay, wound healing, and colony formation assays, respectively. Western blotting and invasion assays were performed to determine expressions and activation of AKT, ERK, p21, and p27. S100A16 was significantly overexpressed in both prostate cancer tissues and cells lines compared to normal controls (P < 0.05). Overexpression of S100A16 significantly promoted invasion, migration, and proliferation in prostate cancer cells in vitro, whereas silencing S100A16 showed the converse effects (P < 0.05). Furthermore, overexpression of S100A16 activated cell signaling proteins AKT and ERK and downregulated tumor suppressors p21 and p27. Specific inhibitors, LY294002 and PD98059, suppressed activation of AKT and ERK, which attenuated DU-145 cell clone formation and invasion induced by S100A16 overexpression. S100A16 may promote human prostate cancer progression via signaling pathways involving AKT, ERK, p21, and p27 downstream effectors. Our findings suggest that S100A16 may serve as a novel therapeutic or diagnostic target in human prostate cancer.

X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user 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 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 17%
Student > Bachelor 3 13%
Student > Master 2 9%
Professor > Associate Professor 2 9%
Professor 1 4%
Other 2 9%
Unknown 9 39%
Readers by discipline Count As %
Medicine and Dentistry 4 17%
Agricultural and Biological Sciences 3 13%
Biochemistry, Genetics and Molecular Biology 2 9%
Neuroscience 2 9%
Computer Science 1 4%
Other 1 4%
Unknown 10 43%
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 07 June 2016.
All research outputs
#18,462,696
of 22,876,619 outputs
Outputs from Tumor Biology
#1,370
of 2,623 outputs
Outputs of similar age
#254,433
of 338,744 outputs
Outputs of similar age from Tumor Biology
#13
of 34 outputs
Altmetric has tracked 22,876,619 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,623 research outputs from this source. They receive a mean Attention Score of 2.3. This one is in the 30th percentile – i.e., 30% 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 338,744 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 34 others from the same source and published within six weeks on either side of this one. This one is in the 32nd percentile – i.e., 32% of its contemporaries scored the same or lower than it.