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Down-regulation of E-cadherin enhances prostate cancer chemoresistance via Notch signaling

Overview of attention for article published in Ai zheng Aizheng Chinese journal of cancer, March 2017
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2 tweeters

Citations

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42 Dimensions

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53 Mendeley
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Title
Down-regulation of E-cadherin enhances prostate cancer chemoresistance via Notch signaling
Published in
Ai zheng Aizheng Chinese journal of cancer, March 2017
DOI 10.1186/s40880-017-0203-x
Pubmed ID
Authors

Wenchu Wang, Lihui Wang, Atsushi Mizokami, Junlin Shi, Chunlin Zou, Jinlu Dai, Evan T. Keller, Yi Lu, Jian Zhang

Abstract

The chemoresistance of prostate cancer (PCa) is invariably associated with the aggressiveness and metastasis of this disease. New emerging evidence indicates that the epithelial-to-mesenchymal transition (EMT) may play pivotal roles in the development of chemoresistance and metastasis. As a hallmark of EMT, E-cadherin is suggested to be a key marker in the development of chemoresistance. However, the molecular mechanisms underlying PCa chemoresistance remain unclear. The current study aimed to explore the association between EMT and chemoresistance in PCa as well as whether changing the expression of E-cadherin would affect PCa chemoresistance. Parental PC3 and DU145 cells and their chemoresistant PC3-TxR and DU145-TxR cells were analyzed. PC3-TxR and DU145-TxR cells were transfected with E-cadherin-expressing lentivirus to overexpress E-cadherin; PC3 and DU145 cells were transfected with small interfering RNA to silence E-cadherin. Changes of EMT phenotype-related markers and signaling pathways were assessed by Western blotting and quantitative real-time polymerase chain reaction. Tumor cell migration, invasion, and colony formation were then evaluated by wound healing, transwell, and colony formation assays, respectively. The drug sensitivity was evaluated using MTS assay. Chemoresistant PC3-TxR and DU145-TxR cells exhibited an invasive and metastatic phenotype that associated with EMT, including the down-regulation of E-cadherin and up-regulation of Vimentin, Snail, and N-cadherin, comparing with that of parental PC3 and DU145 cells. When E-cadherin was overexpressed in PC3-TxR and DU145-TxR cells, the expression of Vimentin and Claudin-1 was down-regulated, and tumor cell migration and invasion were inhibited. In particular, the sensitivity to paclitaxel was reactivated in E-cadherin-overexpressing PC3-TxR and DU145-TxR cells. When E-cadherin expression was silenced in parental PC3 and DU145 cells, the expression of Vimentin and Snail was up-regulated, and, particularly, the sensitivity to paclitaxel was decreased. Interestingly, Notch-1 expression was up-regulated in PC3-TxR and DU145-TxR cells, whereas the E-cadherin expression was down-regulated in these cells comparing with their parental cells. The use of γ-secretase inhibitor, a Notch signaling pathway inhibitor, significantly increased the sensitivity of chemoresistant cells to paclitaxel. The down-regulation of E-cadherin enhances PCa chemoresistance via Notch signaling, and inhibiting the Notch signaling pathway may reverse PCa chemoresistance.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters 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 53 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 53 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 14 26%
Researcher 8 15%
Student > Ph. D. Student 4 8%
Student > Master 4 8%
Student > Doctoral Student 2 4%
Other 9 17%
Unknown 12 23%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 22 42%
Medicine and Dentistry 7 13%
Immunology and Microbiology 2 4%
Agricultural and Biological Sciences 2 4%
Environmental Science 1 2%
Other 3 6%
Unknown 16 30%

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 08 April 2017.
All research outputs
#11,354,779
of 17,522,501 outputs
Outputs from Ai zheng Aizheng Chinese journal of cancer
#134
of 227 outputs
Outputs of similar age
#162,737
of 273,766 outputs
Outputs of similar age from Ai zheng Aizheng Chinese journal of cancer
#1
of 1 outputs
Altmetric has tracked 17,522,501 research outputs across all sources so far. This one is in the 23rd percentile – i.e., 23% of other outputs scored the same or lower than it.
So far Altmetric has tracked 227 research outputs from this source. They receive a mean Attention Score of 4.7. This one is in the 37th percentile – i.e., 37% 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 273,766 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 31st percentile – i.e., 31% of its contemporaries scored the same or lower than it.
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