Integrated analysis reveals CP is a potential biomarker and therapeutic target in glioma

Author:

Liu Linjiang1,Xu Zhen2,Wang Cuicui3,Wu Cheng4,Li Hongjian4,Zhu Qianni4,Gu Dayong5,Zou Haijun6,Li Weihua4

Affiliation:

1. Guangxi University of Chinese Medicine

2. School of Life Science and Technology, ShanghaiTech University

3. Department of ultrasound, Physical examination department, Shenzhen cadre and talent health management center

4. Medical imaging department, Shenzhen Second People’s Hospital/the First Affiliated Hospital of Shenzhen University Health Science Center

5. Department of Laboratory Medicine, Shenzhen Institute of Translational Medicine,The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital

6. Pharmaceutical Department, Shenzhen Second People’s Hospital/the First Affiliated Hospital of Shenzhen University Health Science Center

Abstract

Abstract Purpose: Glioma is a challenging brain tumor with limited treatment options and poor prognosis. Ceruloplasmin (CP), a multicopper protein involved in oxidative stress and iron homeostasis, has been implicated in various cancers but its role in glioma remains unclear. Methods: In this study, we investigated the association between CP expression and various factors, including prognosis, tumor microenvironment (TME), immune infiltration, and immune checkpoint markers. We utilized single-cell sequencing data to assess the expression of CP in both glioma tissues and normal tissues. Furthermore, we conducted in vitro experimentation to evaluate the effects of CP knockdown on glioma cells. Results: Our findings demonstrated a significant correlation between high CP expression and unfavorable clinical characteristics, as well as poor overall survival in glioma patients. Enrichment analysis revealed associations between CP and immune-related pathways, suggesting its involvement in immune regulation. We observed increased immune infiltration in glioma cases exhibiting high CP expression. Additionally, CP expression showed positive correlation with immune checkpoint genes, indicating its potential as an immunotherapy target. Single-cell analysis confirmed the expression of CP in both tumor and immune cells, further supporting its role as a biomarker. Moreover, our in vitro knockdown experiments demonstrated that inhibiting CP suppressed glioma cell proliferation. Conclusion: In summary, our findings suggest that CP is associated with glioma progression, immune regulation, and holds potential therapeutic implications.

Publisher

Research Square Platform LLC

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