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CDDO and ATRA Instigate Differentiation of IMR32 Human Neuroblastoma Cells

Overview of attention for article published in Frontiers in Molecular Neuroscience, September 2017
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Title
CDDO and ATRA Instigate Differentiation of IMR32 Human Neuroblastoma Cells
Published in
Frontiers in Molecular Neuroscience, September 2017
DOI 10.3389/fnmol.2017.00310
Pubmed ID
Authors

Namrata Chaudhari, Priti Talwar, Christian Lefebvre D'hellencourt, Palaniyandi Ravanan

Abstract

Neuroblastoma is the most common solid extra cranial tumor in infants. Improving the clinical outcome of children with aggressive tumors undergoing one of the multiple treatment options has been a major concern. Differentiating neuroblastoma cells holds promise in inducing tumor growth arrest and treating minimal residual disease. In this study, we investigated the effect of partial PPARγ agonist 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO) on human neuroblastoma IMR32 cells. Our results demonstrate that treatment with low concentration of CDDO and particularly in combination with all trans retinoic acid (ATRA) induced neurite outgrowth, increased the percentage of more than two neurites bearing cells, and decreased viability in IMR32 cells. These morphological changes were associated with an increase in expression of bonafide differentiation markers like β3-tubulin and Neuron Specific Enolase (NSE). The differentiation was accompanied by a decrease in the expression of MYCN whose amplification is known to contribute to the pathogenesis of neuroblastoma. MYCN is known to negatively regulate NMYC downstream-regulated gene 1 (NDRG1) in neuroblastomas. MYCN down-regulation induced by CDDO correlated with increased expression of NDRG1. CDDO decreased Anaplastic Lymphoma Kinase (ALK) mRNA expression without affecting its protein level, while ATRA significantly down-regulated ALK. Antagonism of PPARγ receptor by T0070907 meddled with differentiation inducing effects of CDDO as observed by stunted neurite growth, increased viability and decreased expression of differentiation markers. Our findings indicate that IMR32 differentiation induced by CDDO in combination with ATRA enhances, differentiation followed by cell death via cAMP-response-element binding protein (CREB) independent and PPARγ dependent signaling mechanisms.

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The data shown below were collected from the profiles of 3 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 31 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 31 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 10%
Researcher 3 10%
Student > Bachelor 3 10%
Other 2 6%
Lecturer 1 3%
Other 2 6%
Unknown 17 55%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 13%
Medicine and Dentistry 2 6%
Agricultural and Biological Sciences 1 3%
Immunology and Microbiology 1 3%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Other 4 13%
Unknown 18 58%
Attention Score in Context

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 12 October 2017.
All research outputs
#15,480,316
of 23,003,906 outputs
Outputs from Frontiers in Molecular Neuroscience
#1,863
of 2,909 outputs
Outputs of similar age
#200,566
of 320,414 outputs
Outputs of similar age from Frontiers in Molecular Neuroscience
#62
of 115 outputs
Altmetric has tracked 23,003,906 research outputs across all sources so far. This one is in the 22nd percentile – i.e., 22% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,909 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one is in the 28th percentile – i.e., 28% 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 320,414 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 28th percentile – i.e., 28% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 115 others from the same source and published within six weeks on either side of this one. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.