Oncotarget

Research Papers:

CD164 regulates proliferation, progression, and invasion of human glioblastoma cells

Chung-Ching Wang, Dueng-Yuan Hueng, Ai-Fang Huang, Wei-Liang Chen, Shih-Ming Huang _ & James Yi-Hsin Chan _

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Oncotarget. 2019; 10:2041-2054. https://doi.org/10.18632/oncotarget.26724

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Abstract

Chung-Ching Wang1,2, Dueng-Yuan Hueng3,4, Ai-Fang Huang1, Wei-Liang Chen2, Shih-Ming Huang1,3 and James Yi-Hsin Chan1,5,6,7

1 Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

2 Division of Family Medicine, Department of Family and Community Medicine, Tri-Service General Hospital, and School of Medicine, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

3 Department of Biochemistry, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

4 Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

5 Department of Medical Research, Tri-Service General Hospital, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

6 Department of Microbiology and Immunology, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

7 Superintendent’s Office, National Defense Medical Center, Taipei City 114, Taiwan, Republic of China

Correspondence to:

Shih-Ming Huang,email: shihming@ndmctsgh.edu.tw
James Yi-Hsin Chan,email: jchan9473@gmail.com

Keywords: CD164; human glioma; glioblastoma; autophagy

Received: January 18, 2018     Accepted: February 15, 2019     Published: March 12, 2019

ABSTRACT

Grade IV astrocytoma, also known as glioblastoma multiforme (GBM), is the most common and aggressive intracranial glial tumor. GBM is associated with very poor survival and effective treatments have remained elusive so far. Mounting evidence indicates that CD164 contributes to stemness and tumorigenesis in normal cells and is overexpressed in various tumor types, including glioblastoma. Using tissue microarray immunohistochemistry, we show that there is a significant correlation between CD164 expression and glioma type and grade. Depletion of CD164 expression in human glioblastoma cells with siRNA reduced proliferation, migration, and invasiveness. In parallel, immunoblotting showed that downregulation of CD164 expression decreased Akt activation and modified the expression of autophagy markers by upregulating Beclin-1 and LC3B and downregulating p62. These effects were mimicked by inhibition of Akt with MK2206, which suggests that CD164 induces autophagy via Akt/Beclin-1 signaling. We propose that CD164 may serve as a GBM molecular marker and a potential target in therapeutic strategies aimed to improve outcomes for this devastating brain tumor.


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