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Dioxin receptor regulates aldehyde dehydrogenase to block melanoma tumorigenesis and metastasis

Overview of attention for article published in Molecular Cancer, August 2015
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3 tweeters

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28 Dimensions

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45 Mendeley
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Title
Dioxin receptor regulates aldehyde dehydrogenase to block melanoma tumorigenesis and metastasis
Published in
Molecular Cancer, August 2015
DOI 10.1186/s12943-015-0419-9
Pubmed ID
Authors

María Contador-Troca, Alberto Alvarez-Barrientos, Jaime M. Merino, Antonio Morales-Hernández, María I. Rodríguez, Javier Rey-Barroso, Eva Barrasa, María I. Cerezo-Guisado, Inmaculada Catalina-Fernández, Javier Sáenz-Santamaría, Francisco J. Oliver, Pedro M. Fernandez-Salguero

Abstract

The dioxin (AhR) receptor can have oncogenic or tumor suppressor activities depending on the phenotype of the target cell. We have shown that AhR knockdown promotes melanoma primary tumorigenesis and lung metastasis in the mouse and that human metastatic melanomas had reduced AhR levels with respect to benign nevi. Mouse melanoma B16F10 cells were engineered by retroviral transduction to stably downregulate AhR expression, Aldh1a1 expression or both. They were characterized for Aldh1a1 activity, stem cell markers and migration and invasion in vitro. Their tumorigenicity in vivo was analyzed using xenografts and lung metastasis assays as well as in vivo imaging. Depletion of aldehyde dehydrogenase 1a1 (Aldh1a1) impairs the pro-tumorigenic and pro-metastatic advantage of melanoma cells lacking AhR expression (sh-AhR). Thus, Aldh1a1 knockdown in sh-AhR cells (sh-AhR + sh-Aldh1a1) diminished their migration and invasion potentials and blocked tumor growth and metastasis to the lungs in immunocompetent AhR+/+ recipient mice. However, Aldh1a1 downmodulation in AhR-expressing B16F10 cells did not significantly affect tumor growth in vivo. Aldh1a1 knockdown reduced the high levels of CD133(+)/CD29(+)/CD44(+) cells, melanosphere size and the expression of the pluripotency marker Sox2 in sh-AhR cells. Interestingly, Sox2 increased Aldh1a1 expression in sh-AhR but not in sh-AhR + sh-Aldh1a1 cells, suggesting that Aldh1a1 and Sox2 may be co-regulated in melanoma cells. In vivo imaging revealed that mice inoculated with AhR + Aldh1a1 knockdown cells had reduced tumor burden and enhanced survival than those receiving Aldh1a1-expressing sh-AhR cells. Aldh1a1 overactivation in an AhR-deficient background enhances melanoma progression. Since AhR may antagonize the protumoral effects of Aldh1a1, the AhR(low)-Aldh1a1(high) phenotype could be indicative of bad outcome in melanoma.

Twitter Demographics

The data shown below were collected from the profiles of 3 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 45 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 2%
China 1 2%
Unknown 43 96%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 20%
Student > Ph. D. Student 8 18%
Other 3 7%
Student > Master 3 7%
Student > Doctoral Student 2 4%
Other 5 11%
Unknown 15 33%
Readers by discipline Count As %
Agricultural and Biological Sciences 10 22%
Biochemistry, Genetics and Molecular Biology 10 22%
Pharmacology, Toxicology and Pharmaceutical Science 4 9%
Immunology and Microbiology 2 4%
Unspecified 1 2%
Other 4 9%
Unknown 14 31%

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 06 August 2015.
All research outputs
#2,982,338
of 6,334,604 outputs
Outputs from Molecular Cancer
#309
of 650 outputs
Outputs of similar age
#106,191
of 194,974 outputs
Outputs of similar age from Molecular Cancer
#27
of 47 outputs
Altmetric has tracked 6,334,604 research outputs across all sources so far. This one is in the 29th percentile – i.e., 29% of other outputs scored the same or lower than it.
So far Altmetric has tracked 650 research outputs from this source. They receive a mean Attention Score of 3.1. This one is in the 38th percentile – i.e., 38% 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 194,974 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 35th percentile – i.e., 35% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 47 others from the same source and published within six weeks on either side of this one. This one is in the 29th percentile – i.e., 29% of its contemporaries scored the same or lower than it.