↓ Skip to main content

Novel oncogene COPS3 interacts with Beclin1 and Raf-1 to regulate metastasis of osteosarcoma through autophagy

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, July 2018
Altmetric Badge

About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (61st percentile)
  • Good Attention Score compared to outputs of the same age and source (75th percentile)

Mentioned by

twitter
2 X users
patent
1 patent

Citations

dimensions_citation
44 Dimensions

Readers on

mendeley
23 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Novel oncogene COPS3 interacts with Beclin1 and Raf-1 to regulate metastasis of osteosarcoma through autophagy
Published in
Journal of Experimental & Clinical Cancer Research, July 2018
DOI 10.1186/s13046-018-0791-6
Pubmed ID
Authors

Fan Zhang, Taiqiang Yan, Wei Guo, Kunkun Sun, Shidong Wang, Xing Bao, Kuisheng Liu, Bingxin Zheng, Hongliang Zhang, Tingting Ren

Abstract

Expression of COP9 signalosome subunit 3 (COPS3), an oncogene overexpressed in osteosarcoma, has been demonstrated to be significantly correlated with tumor metastasis. However, the underlying mechanism by which COPS3 promotes metastasis of osteosarcoma and its role in autophagy remain unknown. The expression of COPS3 was detected in primary osteosarcoma tissues and matching lung metastasis tissues by immunohistochemistry (IHC). The effect of COPS3 on the metastasis of osteosarcoma cells was investigated by transwell, wound healing assays and animal studies. Indicated proteins was analyzed by western blotting when COPS3 was knockdown or overexpressed. The COPS3 Interacting protein was determined by immunoprecipitation assay. The relationship between COPS3 and autophagy was detected by western blotting and immunofluorescence. We found that knockdown of COPS3 significantly reduced the lung metastasis of osteosarcoma cells in a mouse model, coinciding with downregulation of mitogen-activated protein kinase (MEK) and extracellular signal-regulated kinase (ERK) signaling. The silencing of COPS3 also inhibited the epithelial-mesenchymal transition (EMT) through the 90 kDa ribosomal S6 kinases (RSK), a family of signal transduction proteins downstream of MEK/ERK. Reciprocal immunoprecipitation assays revealed that COPS3 directly interacts with Raf-1, an upstream regulator of MEK/ERK. Surprisingly, Beclin1, an important autophagic protein, appeared in the COPS3-immunoprecipitates, along with the autophagic markers LC3-I and LC3-II. Loss of COPS3 completely inhibited H2O2-induced autophagic flux and reduced Beclin1 expression. Additionally, autophagy inhibitor or silencing of Beclin1 both decreased cell metastasis. Taken together, these data reveal a novel function of COPS3 in the regulation of autophagy and highlight the relationship between autophagy and metastasis in osteosarcoma cells.

X Demographics

X Demographics

The data shown below were collected from the profiles of 2 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 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 5 22%
Student > Ph. D. Student 4 17%
Student > Postgraduate 4 17%
Researcher 2 9%
Student > Master 2 9%
Other 0 0%
Unknown 6 26%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 39%
Medicine and Dentistry 6 26%
Business, Management and Accounting 1 4%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Unknown 6 26%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 4. 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 24 June 2021.
All research outputs
#7,963,683
of 25,385,509 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#505
of 2,382 outputs
Outputs of similar age
#127,736
of 341,301 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#15
of 64 outputs
Altmetric has tracked 25,385,509 research outputs across all sources so far. This one has received more attention than most of these and is in the 67th percentile.
So far Altmetric has tracked 2,382 research outputs from this source. They receive a mean Attention Score of 4.8. This one has done well, scoring higher than 78% 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 341,301 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 61% of its contemporaries.
We're also able to compare this research output to 64 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 75% of its contemporaries.