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Epigenetic down regulation of G protein-coupled estrogen receptor (GPER) functions as a tumor suppressor in colorectal cancer

Overview of attention for article published in Molecular Cancer, May 2017
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  • Above-average Attention Score compared to outputs of the same age (61st percentile)
  • High Attention Score compared to outputs of the same age and source (86th percentile)

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59 Mendeley
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Title
Epigenetic down regulation of G protein-coupled estrogen receptor (GPER) functions as a tumor suppressor in colorectal cancer
Published in
Molecular Cancer, May 2017
DOI 10.1186/s12943-017-0654-3
Pubmed ID
Authors

Qiao Liu, Zhuojia Chen, Guanmin Jiang, Yan Zhou, Xiangling Yang, Hongbin Huang, Huanliang Liu, Jun Du, Hongsheng Wang

Abstract

Estrogenic signals are suggested to have protection roles in the development of colorectal cancer (CRC). The G protein-coupled estrogen receptor (GPER) has been reported to mediate non-genomic effects of estrogen in hormone related cancers except CRC. Its expression and functions in CRC were investigated. The expression of GPER and its associations with clinicopathological features were examined. The mechanisms were further investigated using cells, mouse xenograft models, and clinical human samples. GPER was significantly (p < 0.01) down regulated in CRC tissues compared with their matched adjacent normal tissues in our two cohorts and three independent investigations from Oncomine database. Patients whose tumors expressing less (n = 36) GPER showed significant (p < 0.01) poorer survival rate as compared with those with greater levels of GPER (n = 54). Promoter methylation and histone H3 deacetylation were involved in the down regulation of GPER in CRC cell lines and clinical tissues. Activation of GPER by its specific agonist G-1 inhibited proliferation, induced cell cycle arrest, mitochondrial-related apoptosis and endoplasmic reticulum (ER) stress of CRC cells. The upregulation of reactive oxygen species (ROS) induced sustained ERK1/2 activation participated in G-1 induced cell growth arrest. Further, G-1 can inhibit the phosphorylation, nuclear localization, and transcriptional activities of NF-κB via both canonical IKKα/ IκBα pathways and phosphorylation of GSK-3β. Xenograft model based on HCT-116 cells confirmed that G-1 can suppress the in vivo progression of CRC. Epigenetic down regulation of GPER acts as a tumor suppressor in colorectal cancer and its specific activation might be a potential approach for CRC treatment.

X Demographics

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 59 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 59 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 11 19%
Student > Ph. D. Student 8 14%
Student > Doctoral Student 5 8%
Researcher 5 8%
Student > Postgraduate 4 7%
Other 10 17%
Unknown 16 27%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 19 32%
Medicine and Dentistry 11 19%
Agricultural and Biological Sciences 4 7%
Pharmacology, Toxicology and Pharmaceutical Science 2 3%
Neuroscience 2 3%
Other 5 8%
Unknown 16 27%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 5. 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 22 February 2023.
All research outputs
#7,036,857
of 25,376,589 outputs
Outputs from Molecular Cancer
#558
of 1,915 outputs
Outputs of similar age
#94,598
of 327,237 outputs
Outputs of similar age from Molecular Cancer
#4
of 30 outputs
Altmetric has tracked 25,376,589 research outputs across all sources so far. This one has received more attention than most of these and is in the 71st percentile.
So far Altmetric has tracked 1,915 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.8. This one has gotten more attention than average, scoring higher than 70% 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 327,237 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 61% of its contemporaries.
We're also able to compare this research output to 30 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 86% of its contemporaries.