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The bifunctional autophagic flux by 2-deoxyglucose to control survival or growth of prostate cancer cells

Overview of attention for article published in BMC Cancer, September 2015
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Title
The bifunctional autophagic flux by 2-deoxyglucose to control survival or growth of prostate cancer cells
Published in
BMC Cancer, September 2015
DOI 10.1186/s12885-015-1640-z
Pubmed ID
Authors

Jeong Yong Jeon, Seung Won Kim, Ki Cheong Park, Mijin Yun

Abstract

Recent reports using metabolism regulating drugs showed that nutrient deprivation was an efficient tool to suppress cancer progression. In addition, autophagy control is emerging to prevent cancer cell survival. Autophagy breaks down the unnecessary cytoplasmic components into anabolic units and energy sources, which are the most important sources for making the ATP that maintains homeostasis in cancer cell growth and survival. Therefore, the glucose analog 2-deoxyglucose (2DG) has been used as an anticancer reagent due to its inhibition of glycolysis. Prostate cancer cells (PC3) were treated with 2DG for 6 h or 48 h to analyze the changing of cell cycle and autophagic flux. Rapamycin and LC3B overexpressing vectors were administered to PC3 cells for autophagy induction and chloroquine and shBeclin1 plasmid were used to inhibit autophagy in PC3 cells to analyze PC3 cells growth and survival. The samples for western blotting were prepared in each culture condition to confirm the expression level of autophagy related and regulating proteins. We demonstrated that 2DG inhibits PC3 cells growth and had discriminating effects on autophagy regulation based on the different time period of 2DG treatment to control cell survival. Short-term treatment of 2DG induced autophagic flux, which increased microtubule associated protein 1 light chain 3B (LC3B) conversion rates and reduced p62 levels. However, 2DG induced autophagic flux is remarkably reduced over an extended time period of 2DG treatment for 48 h despite autophagy inducing internal signaling being maintained. The relationship between cell growth and autophagy was proved. Increased autophagic flux by rapamycin or LC3B overexpression powerfully reduced cell growth, while autophagy inhibition with shBeclin1 plasmid or chloroquine had no significant effect on regulating cell growth. Given these results, maintaining increased autophagic flux was more effective at inhibiting cancer cell progression than inhibition of autophagic flux, which is necessary for the survival of PC3 cells. Autophagic flux should be tightly regulated to maintain metabolic homeostasis for cancer cell growth and survival in PC3 cells and is a suitable target for cancer therapy.

Twitter Demographics

The data shown below were collected from the profiles of 2 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 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 7%
Unknown 13 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 43%
Unspecified 2 14%
Professor > Associate Professor 2 14%
Researcher 1 7%
Student > Bachelor 1 7%
Other 2 14%
Readers by discipline Count As %
Agricultural and Biological Sciences 7 50%
Unspecified 2 14%
Biochemistry, Genetics and Molecular Biology 2 14%
Pharmacology, Toxicology and Pharmaceutical Science 1 7%
Neuroscience 1 7%
Other 1 7%

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 20 May 2016.
All research outputs
#5,840,031
of 7,722,452 outputs
Outputs from BMC Cancer
#2,160
of 3,340 outputs
Outputs of similar age
#158,513
of 229,666 outputs
Outputs of similar age from BMC Cancer
#123
of 179 outputs
Altmetric has tracked 7,722,452 research outputs across all sources so far. This one is in the 13th percentile – i.e., 13% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,340 research outputs from this source. They receive a mean Attention Score of 3.4. This one is in the 18th percentile – i.e., 18% of its peers scored the same or lower than it.
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We're also able to compare this research output to 179 others from the same source and published within six weeks on either side of this one. This one is in the 18th percentile – i.e., 18% of its contemporaries scored the same or lower than it.