Identification of monocyte-associated biomarkers in systemic lupus erythematosus and their pan-cancer analysis

Author:

Chen Huiting1ORCID,He Jinxuan23,Wang Linwei1,Lin Yanbin23,Mou Zhixiang23,Huang Xiaoxuan23,Chen Lan123

Affiliation:

1. The School of Clinical Medicine, Fujian Medical University, Fuzhou, China

2. Department of Nephrology, Zhongshan Hospital of Xiamen University, Xiamen, China

3. School of Medicine, Xiamen University, Xiamen, China

Abstract

Immune dysregulation is not only a pathogenic mechanism in systemic lupus erythematosus (SLE) but also a potential cause of the link between SLE and cancer. The current understanding of SLE monocyte-associated biomarkers is limited, and the precise mechanism behind the link between SLE and cancer is uncertain. By using WGCNA and immune infiltration to analyze the GSE72326 dataset, we determined the most pertinent modules for monocytes and discovered eight candidate hub genes from them. The limma software was used to find genes that were differently expressed in SLE. The genes that overlapped between the two were chosen using a Venn diagram as the essential genes related to monocytes in SLE, and the essential genes were verified by several datasets. Correlation analysis and GSEA analysis were used to examine the probable immunological pathways connected to key genes. We examined the expression of hub genes in cancer and their interaction with monocytes using the GEPIA and TIMER databases to understand the significance of essential genes in tumorigenesis. In addition, we performed transcription factor identification. We discovered three biomarkers (IFI30, BLVRA, and RIN2) that are mostly involved in interferon-related signaling pathways and are associated with monocyte-mediated immune responses in SLE. The three important genes are also strongly expressed in a number of malignancies and have a relationship with monocytes. As a result, IFI30, BLVRA, and RIN2 may act as SLE-associated biomarkers of monocytes and as a bridge between SLE and tumors. We proposed that interferon-related signaling pathways might function as possible mediators of cancer risk in SLE.

Funder

Natural Science Foundation of Fujian Province

Natural Science Foundation of Xiamen City

Publisher

SAGE Publications

Subject

Rheumatology

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