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Cancer Manag Res. 2018 Nov 27;10:6409-6419. doi: 10.2147/CMAR.S183293. eCollection 2018.

Specific clinical and immune features of CD68 in glioma via 1,024 samples.

Wang L1,2, Zhang C1,3, Zhang Z1, Han B4, Shen Z1, Li L1,3, Liu S1, Zhao X1, Ye F2, Zhang Y1,3,5.

Author information

1
Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China, yizhang@zzu.edu.cn.
2
Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.
3
Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China, yizhang@zzu.edu.cn.
4
Department of General ICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.
5
Henan Key Laboratory for Tumor Immunology and Biotherapy, Zhengzhou, Henan 450052, China, yizhang@zzu.edu.cn.

Abstract

Background:

There is a growing recognition that tumor-associated macrophages (TAMs) are recruited to the glioma environment, facilitating tumor proliferation and migration by creating an immunosuppressive microenvironment. CD68 has been widely reported as a specific marker of TAMs in cancer.

Purpose:

To clarify the role of CD68 in glioma, we investigated its function at the transcriptome level and relationship with clinical practice.

Patients and methods:

In total, 325 RNA-seq data from Chinese Glioma Genome Atlas (CGGA) and 697 RNA-seq data from The Cancer Genome Atlas (TCGA) network were enrolled in this study. CD68-specific findings were further analyzed with R language, and the prognostic impacts were validated through analyzing the overall survival (OS).

Results:

CD68 showed a positive correlation with the WHO grade of malignancy in glioma. Meanwhile, CD68 was predominantly expressed in IDH wide type and mesenchymal subtype. Gene ontology (GO) analysis revealed that CD68-related genes were closely related to inflammatory response and immune response. Moreover, seven cultures of metagenes further confirmed that CD68 was a specific marker for macrophages in inflammatory response and played an important role in suppressing T-cell-mediated immunity. The Pearson correlation test suggested that CD68 showed robust correlation with other markers of macrophages and immune checkpoints, including PD-1 and TIM-3. Clinically, a high expression level of CD68 in tumors exhibited a poor survival in glioma patients.

Conclusion:

Our results demonstrated that CD68 acted as an immune suppressor and contributed to glioma progression in the tumor microenvironment. These findings may expand our understanding of CD68-specific clinical and immune features in glioma.

KEYWORDS:

CD68; glioma; immunotherapy; tumor-associated macrophage

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

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