Abstract
Caspase recruitment domain-containing protein 9 (CARD9) is highly expressed in myeloid cells and has been identified as a central regulator of innate immunity. Increasingly, studies demonstrate that CARD9 also plays a critical role in the development of lung cancer. This review focuses on the clinical significance and potential molecular mechanisms that CARD9 plays in lung cancer.
Highlights
Through its myeloid cell functions, CARD9 has emerged as an essential player in tumor initiation and progression
We previously summarized the clinical significance of CARD9 in a variety of tumor types (Table 1) including hepatocellular carcinoma, intestinal carcinoma, gastric carcinoma, kidney carcinoma, and malignant pleural effusion [16, 17]
CARD9 is a central integrator of innate immunity in myeloid cells and plays a key role in lung cancer pathogenesis
Summary
CARD9 is highly expressed in myeloid cells especially macrophages, dendritic cells, and MDSCs [14,15,16]. CARD9 is known as the downstream effector molecule of the pattern recognition receptors including Toll-like receptors and C-type Lectins Upon activation of these receptors, CARD9 triggers activation NF-κB and/or mitogenactivated protein kinases (MAPK) signaling in myeloid cells (Fig. 1). We previously summarized the clinical significance of CARD9 in a variety of tumor types (Table 1) including hepatocellular carcinoma, intestinal carcinoma, gastric carcinoma, kidney carcinoma, and malignant pleural effusion [16, 17] These studies suggest that high CARD9 expression is associated with tumor progression and poor survival rate [18,19,20,21,22]. CARD9 inhibited tumor progression in leucocythemia and melanoma by both promoting tumor antigen-specific CD8+ cytotoxic T lymphocyte (CTL) cross-presentation and induction of cancer cell apoptosis [25, 26]. CARD9-induced tumorigenesis was reported in a small cohort of patients, but exact evaluation in a large patient cohort is likely needed to confirm these findings
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