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ARL2 overexpression inhibits glioma proliferation and tumorigenicity via down-regulating AXL

Overview of attention for article published in BMC Cancer, May 2018
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Title
ARL2 overexpression inhibits glioma proliferation and tumorigenicity via down-regulating AXL
Published in
BMC Cancer, May 2018
DOI 10.1186/s12885-018-4517-0
Pubmed ID
Authors

Yulin Wang, Gefei Guan, Wen Cheng, Yang Jiang, Fengping Shan, Anhua Wu, Peng Cheng, Zongze Guo

Abstract

Glioma is the most common primary brain tumor in adults with a poor prognosis. As a member of ARF subfamily GTPase, ARL2 plays a key role in regulating the dynamics of microtubules and mitochondrial functions. Recently, ARL2 has been identified as a prognostic and therapeutic target in a variety range of malignant tumors. However, the biological functional role of ARL2 in glioma still remains unknown. The aim of this study was to explore the expression and functional role of ARL2 in glioma. In this study, we investigated the expression of ARL2 in glioma samples by using RT-PCR, immunohistochemistry and western blot. The correlation between ARL2 expression and the outcomes of glioma patients was evaluated with survival data from TCGA, CGGA and Rembrandt dataset. Lentiviral technique was used for ARL2 overexpression in U87 and U251 cells. CCK8 assay, colony formation assay, wound healing test, transwell invasion assay and in vivo subcutaneous xenograft model were performed to investigated the biological functions of ARL2. ARL2 expression was down-regulated in glioma, and was inversely associated with poor prognosis in glioma patients. Furthermore, exogenous ARL2 overexpression attenuated the growth and colony-formation abilities of glioma cells, as well as their migration and invasive capabilities. Moreover, elevated expression of ARL2 inhibited in vivo tumorigenicity of glioma cells. Mechanistically, ARL2 regulated AXL expression, which was known as an important functional regulator of proliferation and tumorigenicity in glioma cells. Our study suggests that ARL2 inhibits the proliferation, migration and tumorigenicity of glioma cells by regulating the expression of AXL and may conduct as a new prognostic and therapeutic target for glioma.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 19 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 19 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 21%
Researcher 3 16%
Student > Bachelor 2 11%
Professor 1 5%
Student > Master 1 5%
Other 1 5%
Unknown 7 37%
Readers by discipline Count As %
Medicine and Dentistry 5 26%
Pharmacology, Toxicology and Pharmaceutical Science 2 11%
Biochemistry, Genetics and Molecular Biology 1 5%
Social Sciences 1 5%
Engineering 1 5%
Other 0 0%
Unknown 9 47%
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 31 May 2018.
All research outputs
#18,633,675
of 23,083,773 outputs
Outputs from BMC Cancer
#5,469
of 8,378 outputs
Outputs of similar age
#256,005
of 331,250 outputs
Outputs of similar age from BMC Cancer
#113
of 177 outputs
Altmetric has tracked 23,083,773 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 8,378 research outputs from this source. They receive a mean Attention Score of 4.3. This one is in the 21st percentile – i.e., 21% of its peers scored the same or lower than it.
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We're also able to compare this research output to 177 others from the same source and published within six weeks on either side of this one. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.