Abstract
TRIM59 is a protein that is highly expressed in a variety of tumors and promotes tumor development. However, the use of TRIM59 as tumor diagnosis and prognosis biomarker has not been fully explored. We collected datasets from the cancer genome atlas (TCGA) and gene expression omnibus (GEO) to investigate its potential as a biomarker for diagnosis and prognosis. A total of 46 studies, including 11,558 patients were included in this study. Here, we showed that TRIM59 was significantly upregulated in 15 type of human solid tumors in comparison to their adjacent tissues. Receiver operating characteristic curve (ROC) results provided further evidence for the use of TRIM59 as a potential tumor diagnosis biomarker. Overall survival (OS) was compared between TRIM59 high expression and low expression groups. High expression of TRIM59 indicated a poor prognosis in multiple solid tumors. Taken together, these analyses showed that TRIM59 was upregulated in various types of tumors and had the potential to be used as a diagnostic and prognostic biomarker in human solid tumors.
Highlights
Cancer has always been a major global health concern and creates a heavy financial burden for patients and the health care system [1]
We analyzed 15 types of tumor datasets that included sufficient numbers of tumors and adjacent normal tissues in the cancer genome atlas (TCGA), confirming that TRIM59 was highly expressed in tumor samples in comparison to their adjacent tissues (Fig 1)
Thanks to the gene expression data and associated prognosis information provided in public database, we identified that TRIM59 was highly expressed in most solid tumors and could indicate the prognosis in several cancers
Summary
Cancer has always been a major global health concern and creates a heavy financial burden for patients and the health care system [1]. Cancers are always characterized by a group of abnormal expressed genes, and these genes have the potential to be used as diagnosis markers or prognosis predictors [3, 4]. Recent studies have shown that TRIM59 played a role in epigenetic modification [6], embryonic development [7]. Autophagy [8], and was upregulated in multiple tumors [9]. It has been found that downregulation of TRIM59 significantly inhibited tumor growth in vitro experiments and animal models [10, 11]. No large-scale clinical studies have been performed to demonstrate the relationship between TRIM59 and tumor diagnosis and prognosis
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