CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma

Tu,Ming; Cai,Lin; Zheng,Weiming; Su,Zhipeng; Chen,Yong; Qi,Songtao

doi:10.3892/mmr.2017.6204

CD164 regulates proliferation and apoptosis by targeting PTEN in human glioma

Authors:
- Ming Tu
- Lin Cai
- Weiming Zheng
- Zhipeng Su
- Yong Chen
- Songtao Qi
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Affiliations: Department of Neurosurgery, NanFang Hospital of Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China, Department of Neurosurgery, The Second People's Hospital of Yueyang, Yueyang, Hunan 414000, P.R. China
Published online on: February 15, 2017 https://doi.org/10.3892/mmr.2017.6204
Pages: 1713-1721
Copyright: © Tu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cluster of differentiation 164 (CD164), a sialomucin, has been demonstrated to be involved in the regulation of proliferation, apoptosis, adhesion and differentiation in multiple cancers. CD164 is regarded to be a potential promotor of tumor growth. However, the involvement of CD164 in human glioma proliferation and apoptosis remains unknown. The aim of the present study was to investigate the expression and oncogenic function of CD164 in normal human astrocytes (NHA) and glioma cells in vitro and in vivo. The results of the present study demonstrated that CD164 mRNA and protein levels were significantly increased in human glioma cell lines and tissue samples. CD164 overexpression promoted the proliferation of NHA in vitro, and its tumorigenic effect was confirmed in a murine xenograft model. Knockdown of CD164 inhibited cell proliferation and promoted apoptosis of the U87 human glioma cell line in vitro and in vivo. In addition, knockdown of CD164 was demonstrated to upregulate the Bax/Bcl2 ratio and phosphatase and tensin homolog (PTEN) expression, reduce protein kinase B (AKT) phosphorylation and promote the expression of p53 in U87 cells. The results suggest that CD164 expression may have affected the proliferation and apoptosis of human glioma cells via the PTEN/phosphoinositide 3-kinase/AKT pathway, and may therefore present a potential target for the diagnosis and treatment of glioma.

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