A Comprehensive Pan-Cancer Analysis Identifies CEP55 as a Potential Oncogene and Novel Therapeutic Target

Abstract

Emerging research findings have shown that a centrosomal protein (CEP55) is a potential oncogene in numerous human malignancies. Nevertheless, no pan-cancer analysis has been conducted to investigate the various aspects and behavior of this oncogene in different human cancerous tissues. Numerous databases were investigated to conduct a detailed analysis of CEP55. Initially, we evaluated the expression of CEP55 in several types of cancers and attempted to find the correlation between that and the stage of the examined malignancies. Then, we conducted a survival analysis to determine the relationship between CEP55 overexpression in malignancies and the patient’s survival. Furthermore, we examined the genetic alteration forms and the methylation status of this oncogene. Additionally, the interference of CEP55 expression with immune cell infiltration, the response to various chemotherapeutic agents, and the putative molecular mechanism of CEP55 in tumorigenesis were investigated. The current study found that CEP55 was upregulated in cancerous tissues versus normal controls where this upregulation was correlated with a poor prognosis in multiple forms of human cancers. Additionally, it influenced the level of different immune cell infiltration and several chemokines levels in the tumor microenvironment in addition to the response to several antitumor drugs. Herein, we provide an in-depth understanding of the oncogenic activities of CEP55, identifying it as a possible predictive marker as well as a specific target for developing anticancer therapies.

Cancer testis antigens: Emerging therapeutic targets leveraging genomic instability in cancer

“… 218 Likewise, expression of CEP55 has been positively correlated with the expression of more than 30 immune checkpoint genes in a wide range of solid tumors, as well as enhanced infiltration of immunosuppressive myeloid-derived suppressor cells and Th2 cells, expression of immunomodulators and response to immune checkpoint blockade. 219 , 220 , 221 Furthermore, high expression of PBK has been associated with immune escape due to upregulation of PD-L1 expression, dysregulation of antigen presentation and immune cell infiltration. 181 , 222 , 223 , 224 , 225 , 226 Of note, a subcluster of MAGE-A antigens has been reported to predict treatment response of melanoma tumors to immune checkpoint blockade.…”