↓ Skip to main content

Dove Medical Press

Inhibitive effects of 15-deoxy-Δ12,14-prostaglandin J2 on hepatoma-cell proliferation through reactive oxygen species-mediated apoptosis

Overview of attention for article published in OncoTargets and therapy, December 2015
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age
  • Average Attention Score compared to outputs of the same age and source

Mentioned by

googleplus
1 Google+ user

Citations

dimensions_citation
9 Dimensions

Readers on

mendeley
6 Mendeley
Title
Inhibitive effects of 15-deoxy-Δ12,14-prostaglandin J2 on hepatoma-cell proliferation through reactive oxygen species-mediated apoptosis
Published in
OncoTargets and therapy, December 2015
DOI 10.2147/ott.s92832
Pubmed ID
Authors

Kan Chen, Weiqi Dai, Fan Wang, Yujing Xia, Jingjing Li, Sainan Li, Tong Liu, Rong Zhang, Jianrong Wang, Wenxia Lu, Yuqing Zhou, Qin Yin, Yuanyuan Zheng, Huerxidan Abudumijiti, Rongxia Chen, Jie Lu, Yingqun Zhou, Chuanyong Guo

Abstract

15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) induces reactive oxygen species (ROS)-mediated apoptosis in many malignant cells, which has not been studied in hepatoma cells. In this study, we investigated whether 15d-PGJ2 induced apoptosis in hepatocellular carcinoma (HCC) associated with ROS. The LM3, SMMC-7721, and Huh-7 HCC cell lines were treated with 15d-PGJ2 (5-40 μM) for 24, 48, and 72 hours. Cholecystokinin 8 was used to detect the cytotoxicity of 15d-PGJ2. Flow cytometry, Hoechst staining, and Western blotting were used to analyze apoptosis. ROS were combined with the fluorescent probe dihydroethidium and then observed by fluorescence microscopy and flow cytometry. Activation of JNK and expression of Akt were detected by Western blotting. 15d-PGJ2 inhibited HCC cell proliferation and induced apoptosis in a dose- and time-dependent manner. Apoptosis was mainly induced via an intrinsic pathway and was ROS-dependent, and was alleviated by ROS scavengers. ROS induced JNK activation and Akt downregulation in HCC cells. 15d-PGJ2 induced ROS in HCC cell lines, and inhibition of cell growth and apoptosis were partly ROS-dependent.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 6 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 6 100%

Demographic breakdown

Readers by professional status Count As %
Professor 1 17%
Professor > Associate Professor 1 17%
Lecturer > Senior Lecturer 1 17%
Unknown 3 50%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 1 17%
Biochemistry, Genetics and Molecular Biology 1 17%
Medicine and Dentistry 1 17%
Unknown 3 50%
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 December 2015.
All research outputs
#15,351,145
of 22,834,308 outputs
Outputs from OncoTargets and therapy
#1,028
of 2,933 outputs
Outputs of similar age
#227,258
of 387,566 outputs
Outputs of similar age from OncoTargets and therapy
#41
of 91 outputs
Altmetric has tracked 22,834,308 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 2,933 research outputs from this source. They receive a mean Attention Score of 2.6. This one has gotten more attention than average, scoring higher than 54% 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 387,566 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 32nd percentile – i.e., 32% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 91 others from the same source and published within six weeks on either side of this one. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.