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Research Paper

PANX1 is a potential prognostic biomarker associated with immune infiltration in pancreatic adenocarcinoma: A pan-cancer analysis

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Pages 680-696 | Received 19 Aug 2021, Accepted 05 Nov 2021, Published online: 19 Nov 2021
 

ABSTRACT

Pannexin 1 (PANX1) channel is a critical ATP-releasing pathway that modulates tumor immunity, progression, and prognosis. However, the roles of PANX1 in different cancers remain unclear. We analyzed the expression of PANX1 in human pan-cancer in the Oncomine and GEPIA2.0 databases. The prognostic value of PANX1 expression was determined using Kaplan-Meier plotter and OncoLnc tools. The correlation between PANX1 and tumor-infiltrating immune cells was investigated using the TIMER 2.0. In addition, the relationship between PANX1 and immunomodulators was explored using TISIDB. Finally, gene set enrichment analysis (GSEA) was performed utilizing LinkedOmics. The results indicated that PANX1 was overexpressed in most cancers compared to normal tissues. The high expression of PANX1 was associated with poor prognosis in multiple tumors, especially in pancreatic adenocarcinoma (PAAD). In addition, PANX1 was correlated with a variety of immunomodulators, such as CD274, IL10, CD276, IL2RA, TAP1, and TAP2. PANX1 expression level was significantly related to infiltration of multiple immune cells in many cancers, including cancer associated fibroblast, macrophage, and neutrophil cells. Further analysis revealed that PANX1 was significantly associated with T cells CD8+ (rho = 0.524, P = 1.94e-13) and Myeloid dendritic cell (rho = 0.564, P = 9.45e-16). GSEA results showed that PANX1 was closely associated with leukocyte cell-cell adhesion, endoplasmic reticulum lumen, ECM-receptor interaction, and Focal adhesion pathways in PAAD. PANX1 expression was higher in pan-cancer samples than in normal tissues. The high expression of PANX1 was associated with poor outcome and immune infiltration in multiple cancers, especially in PAAD.

Acknowledgments

The present study was supported by the Natural Science Foundation of Ningbo City (2019A610235). We acknowledge TCGA and GEO databases for providing their platforms, as well as contributors for uploading important datasets.

Disclosure statement

TCGA and GEO are public databases. The patients who are part of the database have obtained ethical approval. Users can download pertinent data for free for research and publish relevant articles. Because our study is based on open-source data, there are no ethical issues or conflicts of interest. The authors declare that they have no competing interests.

Authors’ contributions

LB and KS performed data analysis. LB and KS prepared the manuscript. XZ designed the study. All authors read and approved the final manuscript.

Additional information

Funding

This work was supported by the Natural Science Foundation of Ningbo City [2019A610235].