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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.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 19%
Researcher 3 14%
Student > Bachelor 2 10%
Student > Master 2 10%
Professor 1 5%
Other 2 10%
Unknown 7 33%
Readers by discipline Count As %
Medicine and Dentistry 6 29%
Pharmacology, Toxicology and Pharmaceutical Science 2 10%
Biochemistry, Genetics and Molecular Biology 1 5%
Unspecified 1 5%
Social Sciences 1 5%
Other 1 5%
Unknown 9 43%

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
#10,383,099
of 13,017,042 outputs
Outputs from BMC Cancer
#3,224
of 4,856 outputs
Outputs of similar age
#203,495
of 271,669 outputs
Outputs of similar age from BMC Cancer
#1
of 1 outputs
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