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American Association for Cancer Research

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Mitochondrial β-Carotene 9′,10′ Oxygenase Modulates Prostate Cancer Growth via NF-κB Inhibition: A Lycopene-Independent Function

Overview of attention for article published in Molecular Cancer Research, July 2016
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (92nd percentile)
  • High Attention Score compared to outputs of the same age and source (95th percentile)

Mentioned by

news
2 news outlets
blogs
1 blog
twitter
1 tweeter

Citations

dimensions_citation
39 Dimensions

Readers on

mendeley
40 Mendeley
Title
Mitochondrial β-Carotene 9′,10′ Oxygenase Modulates Prostate Cancer Growth via NF-κB Inhibition: A Lycopene-Independent Function
Published in
Molecular Cancer Research, July 2016
DOI 10.1158/1541-7786.mcr-16-0075
Pubmed ID
Authors

Xiaoming Gong, Raju Marisiddaiah, Susan Zaripheh, Doris Wiener, Lewis P. Rubin

Abstract

Despite numerous inquiries into protective roles of lycopene in prostate cancer (PCa) prevention or therapy, little is known about mechanisms by which lycopene or its metabolites inhibit PCa. The enzyme beta-carotene 9,10'-oxygenase (BCO2), which catalyzes asymmetric cleavage of several carotenoids, is the principal regulator of lycopene metabolism, but the range of BCO2 biological functions is incompletely understood. This study investigated expression and functional roles of BCO2 in human PCa. Expression of the bco2 gene is dramatically decreased in PCa tissue and in a range of PCa cell lines as compared to non-neoplastic prostate tissue and normal prostatic epithelial cells, respectively. Inhibition of DNA methyltransferase activity restored bco2 expression in PCa cell lines tested. Treatment with lycopene or its metabolite, apo-10-lycopenal, also increased bco2 expression and 31 reduced cell proliferation in androgen-sensitive cell lines, but lycopene neither altered bco2 expression nor cell growth in androgen-resistant cells. Notably, restoring bco2 expression in PCa cells inhibited cell proliferation and colony formation, irrespective of lycopene exposure. Exogenous expression of either wild-type BCO2 or a mutant (enzymatically inactive) BCO2 in PCa cells reduced nuclear factor kappa B (NF-B) activity and decreased NF-B nuclear translocation and DNA binding. Together, these results indicate epigenetic loss of BCO2 expression is associated with prostate cancer progression. Moreover, these findings describe previously unanticipated functions of BCO2 that are independent of its enzymatic role in lycopene metabolism. This study identifies BCO2 as a tumor suppressor in prostate cancer. BCO2-mediated inhibition of NF-kappaB signaling implies BCO2 status is important in prostate cancer progression.

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

Geographical breakdown

Country Count As %
Spain 1 3%
Unknown 39 98%

Demographic breakdown

Readers by professional status Count As %
Student > Master 11 28%
Professor 5 13%
Researcher 5 13%
Student > Bachelor 4 10%
Student > Ph. D. Student 4 10%
Other 7 18%
Unknown 4 10%
Readers by discipline Count As %
Medicine and Dentistry 9 23%
Biochemistry, Genetics and Molecular Biology 6 15%
Agricultural and Biological Sciences 5 13%
Pharmacology, Toxicology and Pharmaceutical Science 4 10%
Nursing and Health Professions 3 8%
Other 5 13%
Unknown 8 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 24. 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 28 October 2021.
All research outputs
#1,109,067
of 19,508,584 outputs
Outputs from Molecular Cancer Research
#56
of 1,676 outputs
Outputs of similar age
#21,510
of 269,521 outputs
Outputs of similar age from Molecular Cancer Research
#2
of 20 outputs
Altmetric has tracked 19,508,584 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 94th percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,676 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.6. This one has done particularly well, scoring higher than 96% 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 269,521 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 92% of its contemporaries.
We're also able to compare this research output to 20 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 95% of its contemporaries.