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Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21waf-1

Overview of attention for article published in GeroScience, May 2016
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Title
Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21waf-1
Published in
GeroScience, May 2016
DOI 10.1007/s11357-016-9922-1
Pubmed ID
Authors

Souneek Chakraborty, Reyaz ur Rasool, Sunil Kumar, Debasis Nayak, Bilal Rah, Archana Katoch, Hina Amin, Asif Ali, Anindya Goswami

Abstract

Stress-induced premature senescence (SIPS) is quite similar to replicative senescence that is committed by cells exposed to various stress conditions viz. ultraviolet radiation (DNA damage), hydrogen peroxide (oxidative stress), chemotherapeutic agents (cytotoxic threat), etc. Here, we report that cristacarpin, a natural product obtained from the stem bark of Erythrina suberosa, promotes endoplasmic reticulum (ER) stress, leading to sub-lethal reactive oxygen species (ROS) generation and which eventually terminates by triggering senescence in pancreatic and breast cancer cells through blocking the cell cycle in the G1 phase. The majority of cristacarpin-treated cells responded to conventional SA-β-gal stains; showed characteristic p21(waf1) upregulation along with enlarged and flattened morphology; and increased volume, granularity, and formation of heterochromatin foci-all of these features are the hallmarks of senescence. Inhibition of ROS generation by N-acetyl-L-cysteine (NAC) significantly reduced the expression of p21(waf1), confirming that the modulation in p21(waf1) by anti-proliferative cristacarpin was ROS dependent. Further, the elevation in p21(waf1) expression in PANC-1 and MCF-7 cells was consistent with the decrease in the expression of Cdk-2 and cyclinD1. Here, we provide evidence that cristacarpin promotes senescence in a p53-independent manner. Moreover, cristacarpin treatment induced p38MAPK, indicating the ROS-dependent activation of the MAP kinase pathway, and thus abrogates the tumor growth in mouse allograft tumor model.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 22%
Student > Bachelor 4 15%
Researcher 4 15%
Lecturer 2 7%
Student > Doctoral Student 2 7%
Other 4 15%
Unknown 5 19%
Readers by discipline Count As %
Agricultural and Biological Sciences 6 22%
Biochemistry, Genetics and Molecular Biology 5 19%
Medicine and Dentistry 4 15%
Chemistry 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Other 5 19%
Unknown 4 15%
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 02 June 2016.
All research outputs
#22,758,309
of 25,373,627 outputs
Outputs from GeroScience
#1,512
of 1,594 outputs
Outputs of similar age
#309,337
of 353,676 outputs
Outputs of similar age from GeroScience
#14
of 14 outputs
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So far Altmetric has tracked 1,594 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 17.0. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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