BMC Bioinformatics (Sep 2022)

A pan-cancer analysis of collagen VI family on prognosis, tumor microenvironment, and its potential therapeutic effect

  • Xiang Li,
  • Zeng Li,
  • Shanzhi Gu,
  • Xinhan Zhao

DOI
https://doi.org/10.1186/s12859-022-04951-0
Journal volume & issue
Vol. 23, no. 1
pp. 1 – 15

Abstract

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Abstract Background Collagen VI family (COL6A) is a major member of extracellular matrix protein. There is accumulating evidence that COL6A is involved in tumorigenesis and tumor progression. In this study, we performed a systematic analysis of COL6A in pan-cancer based on their molecular features and clinical significance. Methods Based on updated public databases, we integrated several bioinformatics analysis methods to investigate the expression levels of COL6A as well as the relationship between their expression and patient survival, immune subtypes, tumor microenvironment, stemness scores, drug sensitivity, and DNA methylation. Results The expression levels of COL6A members varied in different cancers, suggesting their expression was cancer-dependent. Among COL6A members, COL6A1/2/3 were predicted poor prognosis in specific cancers. Furthermore, COL6A1/2/3 expression levels revealed a clear correlation with immune subtypes, and COL6A1/2/3 were associated with tumor purity, that is, gene expression levels were generally higher in tumors with higher stromal scores and immune scores. COL6A1/2/3 had a significantly negative correlation with RNA stemness scores, and meanwhile they were also related to DNA stemness scores in different degrees. In addition, the expression of COL6A1/2/3 was significantly related to drug sensitivity of cancer cells. Finally, our study revealed that COL6A1/2/3 expression was mainly negatively correlated with gene methylation, and the methylation levels showed remarkable differences in various cancers. Conclusions These findings highlight both the similarities and differences in the molecular characteristics of COL6A members in pan-cancer, and provide comprehensive insights for further investigation into the mechanism of COL6A.

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