Researchers identified 5 hub genes common to patients with idiopathic pulmonary fibrosis (IPF) and nonsmall cell lung cancer (NSCLC), which is a common complication of IPF, and published their results in Frontiers in Genetics. These results offer potential therapeutic targets for patients with IPF as well as insights into the underlying mechanisms of both diseases.

“In our study, we applied bioinformatics algorithms to explore the common hub genes and biological pathways associated with IPF and lung cancer progression,” the authors wrote.

“The findings from this study may increase the understanding of the underlying molecular mechanisms of IPF and lung cancer and identify new targets for the development of new therapeutic agents for patients with IPF and coexisting lung cancer.”

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The research team retrieved gene expression data on samples from 119 patients with IPF and normal healthy lung tissue from the Gene Expression Omnibus and Cancer Genome Atlas databases. They then identified the hub genes using a new plug-in called CytoHubba within the Cytoscape v3.7.2 software program. Next, they utilized R software to construct a diagnostic nomogram that was validated in another IPF dataset as having a good diagnostic ability for NSCLC cohorts.

The survival analysis revealed that elevated levels of cancer-associated fibroblasts were correlated with poor overall survival and disease-free survival, suggesting that antifibrosis therapy might slow cancer progression. The authors postulate that the success of their nomogram could be due to IPF acting as a precancerous manifestation of lung cancer, which could evolve into cancer over time.

In addition, fibroblasts play a major role in both IPF and carcinogenesis, and the 5 identified hub genes all promote fibroblast accumulation and therefore could serve as candidate target genes for therapy.


Yao Y, Li Z, Gao W. Identification of hub genes in idiopathic pulmonary fibrosis and NSCLC progression: evidence from bioinformatics analysis. Front Genet. Published online April 11, 2022. doi:10.3389/fgene.2022.855789