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Thymoquinone suppression of the human hepatocellular carcinoma cell growth involves inhibition of IL-8 expression, elevated levels of TRAIL receptors, oxidative stress and apoptosis

Overview of attention for article published in Molecular and Cellular Biochemistry, January 2014
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (58th percentile)
  • High Attention Score compared to outputs of the same age and source (84th percentile)

Mentioned by

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3 tweeters

Citations

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29 Dimensions

Readers on

mendeley
21 Mendeley
Title
Thymoquinone suppression of the human hepatocellular carcinoma cell growth involves inhibition of IL-8 expression, elevated levels of TRAIL receptors, oxidative stress and apoptosis
Published in
Molecular and Cellular Biochemistry, January 2014
DOI 10.1007/s11010-013-1930-1
Pubmed ID
Authors

Abdelkader E. Ashour, Adel R. Abd-Allah, Hesham M. Korashy, Sabry M. Attia, Abdelrahman Z. Alzahrani, Quaiser Saquib, Saleh A. Bakheet, Hala E. Abdel-Hamied, Shazia Jamal, Arun K. Rishi

Abstract

Hepatocellular carcinoma (HCC) is the fourth most common solid tumor worldwide. The chemokine interleukin-8 (IL-8) is overexpressed in HCC and is a potential target for therapy. Although the transcription factor NF-κB regulates IL-8 expression, and while thymoquinone (TQ; the most bioactive constituent of black seed oil) inhibits NF-κB activity, the precise mechanisms by which TQ regulates IL-8 and cancer cell growth remain to be clarified. Here, we report that TQ inhibited growth of HCC cells in a dose- and time-dependent manner, caused G2M cell cycle arrest, and stimulated apoptosis. Apoptosis was substantiated by activation of caspase-3 and -9, as well as cleavage of poly(ADP-ribose)polymerase. TQ treatments inhibited expression of NF-κB and suppressed IL-8 and its receptors. TQ treatments caused increased levels of reactive oxygen species (ROS) and mRNAs of oxidative stress-related genes, NQO1 and HO-1. Pretreatment of HepG2 cells with N-acetylcysteine, a scavenger of ROS, prevented TQ-induced cell death. TQ treatment stimulated mRNA expression of pro-apoptotic Bcl-xS and TRAIL death receptors, and inhibited expression of the anti-apoptotic gene Bcl-2. TQ enhanced TRAIL-induced death of HepG2 cells, in part by up-regulating TRAIL death receptors, inhibiting NF-κB and IL-8 and stimulating apoptosis. Altogether, these findings provide insights into the pleiotropic molecular mechanisms of TQ-dependent suppression of HCC cell growth and underscore potential of this compound as anti-HCC drug.

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

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Unspecified 3 14%
Professor 3 14%
Student > Ph. D. Student 3 14%
Student > Master 3 14%
Student > Bachelor 3 14%
Other 6 29%
Readers by discipline Count As %
Medicine and Dentistry 5 24%
Unspecified 5 24%
Biochemistry, Genetics and Molecular Biology 5 24%
Agricultural and Biological Sciences 3 14%
Chemistry 1 5%
Other 2 10%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 November 2014.
All research outputs
#2,523,720
of 6,229,690 outputs
Outputs from Molecular and Cellular Biochemistry
#388
of 881 outputs
Outputs of similar age
#54,900
of 133,514 outputs
Outputs of similar age from Molecular and Cellular Biochemistry
#3
of 19 outputs
Altmetric has tracked 6,229,690 research outputs across all sources so far. This one has received more attention than most of these and is in the 59th percentile.
So far Altmetric has tracked 881 research outputs from this source. They receive a mean Attention Score of 3.4. This one has gotten more attention than average, scoring higher than 55% 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 133,514 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 58% of its contemporaries.
We're also able to compare this research output to 19 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.