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Endothelial-Monocyte Activating Polypeptide II Suppresses the In Vitro Glioblastoma-Induced Angiogenesis by Inducing Autophagy

Overview of attention for article published in Frontiers in Molecular Neuroscience, June 2017
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Title
Endothelial-Monocyte Activating Polypeptide II Suppresses the In Vitro Glioblastoma-Induced Angiogenesis by Inducing Autophagy
Published in
Frontiers in Molecular Neuroscience, June 2017
DOI 10.3389/fnmol.2017.00208
Pubmed ID
Authors

Zhiqing Li, Jun Ma, Libo Liu, Xiaobai Liu, Ping Wang, Yunhui Liu, Zhen Li, Jian Zheng, Jiajia Chen, Wei Tao, Yixue Xue

Abstract

The obstacle in delivering therapeutics to glioblastoma (GBM) is tumor-induced angiogenesis which leads to the formation of abnormal vessels and a dysfunctional blood-tumor barrier. Here, we elucidated the effect of endothelial-monocyte activating polypeptide II (EMAP II) on the GBM-induced angiogenesis as well as its potential mechanisms. Our results proved that EMAP II inhibited the viability, mitochondrial membrane potential, migration and tube formation of GBM-induced endothelial cells (GECs) by inducing cell autophagy, demonstrated by cell viability assay, JC-1 staining assay, transwell assay and tube formation assay, respectively. Cell autophagy was induced by EMAP II through the observation of autophagic vacuoles formation and the up-regulation of microtubule-associated protein-1 light chain-3 (LC3)-II and p62/SQSTM1 expression, demonstrated by transmission electron microscopy analysis, immunofluorescence assay and Western blot assay. The activity of PI3K/AKT/mTOR signal pathway could be inhibited by the EMAP II treatment. Furthermore, unfolded protein response (UPR)-related proteins (GRP78, eIF2α, and CHOP) were up-regulated by EMAP II, which suggest that GECs exposed to EMAP II experienced endoplasmic reticulum stress. Further, mechanistic investigations found that EMAP II reduced the miR-96 expression which could directly target the 3'-UTR of these UPR-related proteins, and over-expression of miR-96 inhibited LC3 and p62/SQSTM1 expression by down-regulating these UPR-related proteins in GECs. Moreover, the combination of EMAP II with miR-96 inhibitor showed the inhibitory effect on the viability, migration, and in vitro tube formation of GECs, which are critical for angiogenesis. Taken together, we have demonstrated the fact that EMAP II resulted in the decreased GBM-induced angiogenesis by inducing autophagy, which might contribute to establishing potential strategies for human GBM treatment.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 11 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 11 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 3 27%
Researcher 2 18%
Student > Doctoral Student 1 9%
Student > Master 1 9%
Student > Ph. D. Student 1 9%
Other 0 0%
Unknown 3 27%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 45%
Medicine and Dentistry 3 27%
Agricultural and Biological Sciences 1 9%
Unknown 2 18%
Attention Score in Context

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 28 July 2017.
All research outputs
#15,967,503
of 25,703,943 outputs
Outputs from Frontiers in Molecular Neuroscience
#1,697
of 3,372 outputs
Outputs of similar age
#182,303
of 329,296 outputs
Outputs of similar age from Frontiers in Molecular Neuroscience
#55
of 116 outputs
Altmetric has tracked 25,703,943 research outputs across all sources so far. This one is in the 36th percentile – i.e., 36% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,372 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.3. This one is in the 46th percentile – i.e., 46% of its peers scored the same or lower than it.
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 329,296 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 43rd percentile – i.e., 43% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 116 others from the same source and published within six weeks on either side of this one. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.