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Testis specific Y-like 5: gene expression, methylation and implications for drug sensitivity in prostate carcinoma

Overview of attention for article published in BMC Cancer, February 2017
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • One of the highest-scoring outputs from this source (#10 of 5,069)
  • High Attention Score compared to outputs of the same age (97th percentile)

Mentioned by

news
15 news outlets
blogs
2 blogs
twitter
1 tweeter
facebook
1 Facebook page
wikipedia
1 Wikipedia page

Citations

dimensions_citation
8 Dimensions

Readers on

mendeley
13 Mendeley
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Title
Testis specific Y-like 5: gene expression, methylation and implications for drug sensitivity in prostate carcinoma
Published in
BMC Cancer, February 2017
DOI 10.1186/s12885-017-3134-7
Pubmed ID
Authors

Senthil R. Kumar, Jeffrey N. Bryan, Magda Esebua, James Amos-Landgraf, Tanner J. May

Abstract

TSPYL5, a putative tumor suppressor gene, belongs to the nucleosome assembly protein family. The chromosomal location of the TSPYL5 gene is 8Q22.1, and its exact role in prostate cancer etiology remains unclear. Further TSPYL5 gene and protein expression in prostate carcinoma cells and diseased tissues including its susceptibility for epigenetic silencing is unknown. Also, not known is the variation in TSPYL5 protein expression with regards to progression of prostatic carcinoma and its possible role in drug sensitivity. TSPYL5, DNMT-1 and DNMT-B gene expression in DU145, LNCaP and RWPE-1 cells and prostate tumor tissues was analyzed by qRT-PCR and RT-PCR. Demethylation experiments were done by treating DU145 and LNCaP cells with 5-aza-2'-deoxycytidine in vitro. Methylation analysis of TSPYL5 gene was performed by methylation specific PCR and pyrosequencing. TSPYL5 protein expression in benign and diseased prostate tumor tissues was performed by immunohistochemistry and in the cells by Western blotting. TSPYL5 was differentially expressed in non-tumorigenic prostate epithelial cells (RWPE-1), androgen independent (DU145), dependent (LNCaP) prostate carcinoma cells and tissues. Methylation-specific PCR and pyrosequencing analysis identified an inverse relationship between DNA methylation and expression leading to the silencing of TSPYL5 gene. Treatment of prostate carcinoma cells in which TSPYL5 was absent or low (DU145 and LNCaP) with the demethylating agent 5-aza-2'-deoxycytidine upregulated its expression in these cells. Immunohistochemical studies clearly identified TSPYL5 protein in benign tissue and in tumors with Gleason score (GS) of 6 and 7. TSPYL5 protein levels were very low in tumors of GS ≥ 8. TSPYL5 overexpression in LNCaP cells increased the cell sensitivity to chemotherapy drugs such as docetaxel and paclitaxel, as measured by the cellular viability. Furthermore, the cells also exhibited reduced CDKN1A expression with only marginal reduction in pAKT. Decrease in TSPYL5 protein in advanced tumors might possibly function as an indicator of prostate tumor progression. Its absence due to methylation-induced silencing can lead to reduced drug sensitivity in prostate carcinoma.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 13 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 13 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 3 23%
Student > Bachelor 2 15%
Professor 1 8%
Other 1 8%
Student > Ph. D. Student 1 8%
Other 2 15%
Unknown 3 23%
Readers by discipline Count As %
Medicine and Dentistry 3 23%
Biochemistry, Genetics and Molecular Biology 3 23%
Agricultural and Biological Sciences 2 15%
Immunology and Microbiology 1 8%
Veterinary Science and Veterinary Medicine 1 8%
Other 0 0%
Unknown 3 23%

Attention Score in Context

This research output has an Altmetric Attention Score of 125. 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 06 September 2018.
All research outputs
#119,675
of 13,477,526 outputs
Outputs from BMC Cancer
#10
of 5,069 outputs
Outputs of similar age
#5,471
of 258,483 outputs
Outputs of similar age from BMC Cancer
#1
of 1 outputs
Altmetric has tracked 13,477,526 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 99th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 5,069 research outputs from this source. They receive a mean Attention Score of 4.0. This one has done particularly well, scoring higher than 99% of its peers.
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 258,483 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 97% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them