622P - A prognostic and immune infiltration analysis of CCL26 in pan-cancer

Background

CCL26 is widely found in various tissues of the human body and mainly acts on eosinophils. However, its role in tumors remains unclear. In this study, we aimed to investigate the role of CCL26 in pan-cancer.

Methods

Data were downloaded from University of California Santa Cruz (UCSC) Xena and The Cancer Genome Atlas (TCGA). The expression of CCL26 was investigated in TCGA_GTEx, TCGA and TCGA paired samples, respectively. Subsequently, Kaplan-Meier analyses were performed on 33 TCGA tumors, and clinical correlation and one-way Cox regression analyses were performed on tumors in which CCL26 affected prognosis. In addition, we selected more than 500 representative tumors of renal clear cell carcinoma (KIRC) to construct a nomogram model to confirm the prognostic value of CCL26 in the tumors. In addition, CCL26 there was an association with immune cell infiltration. Mechanistically, we performed functional enrichment analysis to explore potential signaling pathways in which CCL26 may be involved.

Results

Our study found that CCL26 expression was significantly up-regulated in 20 tumors and down-regulated in 6. High expression of CCL26 was associated with shorter overall survival (OS) in adrenocortical carcinoma (ACC), bladder uroepithelial carcinoma (BLCA), renal clear cell carcinoma (KIRC), papillary renal cell carcinoma (KIRP), and mesothelioma (MESO). CCL26 had high predictive accuracy (AUC > 0.9) for five cancers, including cholangiocarcinoma (CHOL; AUC = 0.952, CI: 0.890-0=1.000), renal smoky cell carcinoma (KICH; AUC = 0.928, CI: 0.875- 0.981), lung squamous cell carcinoma (LUSC; AUC = 0.928, CI: 0.905-0.951), skin melanoma (SKCM; AUC = 0.936, CI: NA-NA), thymoma (THYM; AUC = 0.933, CI: 0.829-1.000). -1.000).

Conclusions

CCL26 may serve as a potential prognostic biomarker and a promising target for cancer immunotherapy. It is also associated with clinical outcomes and immune microenvironment in a variety of tumors, and may influence tumor development by regulating signaling pathways of stem cell pluripotency and immune-related pathways.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.