ABSTRACT
The extracellular matrix (ECM) shows an essential effect during the occurrence and procession of human cancers. Type III collagen is a crucial component of ECM. Collagen Type III Alpha 1(COL3A1) is aberrantly expressed in a variety of cancers. Nevertheless, the role of COL3A1 in pan-cancer stays unidentified. In this study, we explored public databases, including Cancer Genome Atlas (TCGA), GTEx, GEPIA, cBioPortal, Oncommine, TIMER and GENEMANIA databases to identify the differential expression of COL3A1 in human cancer tissues and normal samples, followed by its prognostic value for patient survival. In addition, we explore the association between COL3A1 expression and immune infiltration. Further, we used the GeneMANIA database and Gene Set Enrichment Analysis (GSEA) to investigate Protein–Protein Interaction (PPI) and gene functional enrichment. Results show that COL3A1 expressed higher in tumor samples than in normal samples. Upregulation of COL3A1 is associated with a worse prognosis and a more advanced cancer stage. COL3A1 expression shows significant positive correlations with tumor-infiltrating immune cells (TIICs), including neutrophils, macrophages, CD8 + T cells, CD4 + T cells, dendritic cells, and B cells. Markers of TIICs demonstrated distinct patterns of COL3A1-related immune infiltration. COL3A1 expression was associated with ECM receptor interaction, regulation of actin cytoskeleton and focal adhesion pathways via GSEA analysis. In conclusion, COL3A1 may be a molecular biomarker for prognosis and immune infiltration in pan-cancer. It might act as a potential target for a new insight of human cancers management.
Acknowledgements
We are grateful to TCGA and GTEx databases for their availability and contributors for providing their valuable datasets. We appreciate the aforementioned online databases and platforms for their selfless sharing and technical support.
Disclosure statement
The authors do not have a conflict of interest.
Data availability statement
This study analyzed publicly available datasets. All raw data were available from TCGA(https://portal.gdc.cancer.gov/).
Author contributions
D-MH performed the design of this research. Z-HY and DC drafted the manuscript and analyzed the results. DC, L-YT, CX, and W-SD acquired and analyzed the data. C-LX, Z-HY, L-PY, and Y-ZP helped discuss the results. D-MH and Z-HY revised the manuscript. All authors contributed to this article and gave approval for the submission.
Supplementary material
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