As part of the tumor microenvironment (TME),
collagen plays a significant role in
cancer fibrosis formation. However, the
collagen family expression profile and clinical features in
lung adenocarcinoma (LUAD) are poorly understood. The objective of the present work was to investigate the expression pattern of genes from the
collagen family in LUAD and to develop a predictive signature based on
collagen family. The
Cancer Genome Atlas (TCGA) samples were used as the training set, and five additional cohort samples obtained from the Gene Expression Omnibus (GEO) database were used as the validation set. A predictive model based on five
collagen genes, including COL1A1, COL4A3, COL5A1, COL11A1, and COL22A1, was created by analyzing samples from the TCGA cohort using LASSO Cox analysis and univariate/multivariable Cox regression. Using
Collagen-Risk scores, LUAD patients were then divided into high- and low-risk groups. KM survival analysis showed that
collagen signature presented a robust prognostic power. GO and KEGG analyses confirmed that
collagen signature was associated with extracellular matrix organization, ECM-receptor interaction, PI3K-Akts and AGE-RAGE signaling activation. High-risk patients exhibited a considerable activation of the p53 pathway and cell cycle, according to GSEA analysis. The Collage-Risk model showed unique features in immune cell infiltration and tumor-associated macrophage (TAM) polarization of the TME. Additionally, we deeply revealed the association of
collagen signature with immune checkpoints (ICPs),
tumor mutation burden (TMB), and
tumor purity. We first constructed a reliable prognostic model based on TME principal component-
collagen, which would enable clinicians to treat patients with LUAD more individually.