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pmid:34734011

Bioinformatic analysis of differentially expressed genes and pathways in idiopathic pulmonary fibrosis.

Nana Li · Lingxiao Qiu · Cheng Zeng · Zeming Fang · Shanshan Chen · Xiangjin Song · Heng Song · Guojun Zhang

Annals of translational medicine · 2021 doi:10.21037/atm-21-4224

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Experiment

complete

Data

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absent

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title
Bioinformatic analysis of differentially expressed genes and pathways in idiopathic pulmonary fibrosis.
doi
10.21037/atm-21-4224
pmid
34734011
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[0]
Nana Li
[1]
Lingxiao Qiu
[2]
Cheng Zeng
[3]
Zeming Fang
[4]
Shanshan Chen
[5]
Xiangjin Song
[6]
Heng Song
[7]
Guojun Zhang
journal
Annals of translational medicine
year
2021
abstract
BACKGROUND: Using bioinformatic methods to explore the differentially expressed genes (DEGs) of human idiopathic pulmonary fibrosis (IPF) and to elucidate the pathogenesis of IPF from the genetic level. METHODS: The GSE110147 gene expression profile was downloaded from the GEO database. The data of lung adenocarcinoma (LUAD) samples, lung squamous cell carcinoma (LUSC) samples and normal samples were downloaded from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. DEGs between IPF patients and healthy donors were analyzed using the GEO2R tool. Use the "clusterprofiler" package in R software to perform gene ontology (GO) and KEGG pathway enrichment analysis, and then perform function annotation and protein-protein interaction (PPI) network construction in the STRING online tool. The Genome Browser tool of the university of california santa cruz (UCSC) online website was used to predict transcription factors (TFs) of genes. In the final, the results were analyzed synthetically. RESULTS: A total of 9,183 DEGs were identified, of which 4,545 genes were down-regulated, and 4638 were up-regulated. MMP1, SPP1, and BPIFB1 were the top three DEGs with the highest significant up-regulation. These DEGs played an important role in the occurrence of IPF through the MAPK (mitogen-activated protein kinase) signaling pathway. Furthermore, 50 DEGs were enriched in the expression of PD-L1 and the PD-1 checkpoint pathway in cancer, of which 11 genes were re-enriched in the pathway of non-small cell lung cancer. The expression of the 11 genes were extensively regulated by CTCFL, SP2 and ZNF341. Most of them were differentially expressed between lung cancers and normal lung tissues. The overall survival (OS) curve of LUAD were significantly stratified by AKT2, KRAS, PIK3R1, meanwhile the OS curve of LUAC was significantly stratified by MAPK3. CONCLUSIONS: Bioinformatics analysis revealed that DEGs including MPP1 might be potential targets and biomarkers of IPF, and the MAPK signaling pathway is related to the occurrence and development of IPF. The development of IPF lung cancer complications may be related to the activation of genes enriched in PD-L1 expression and PD-1 checkpoint pathway, which provides clues to the pathogenesis of IPF combined with lung cancer.
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GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r) was used to detect differentially expressed genes (DEGs) of IPF compared to normal tissues. The screening condition was P<0.05 and |log fold change| >0.5.
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GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r) was used to detect differentially expressed genes (DEGs) of IPF compared to normal tissues. The screening condition was P<0.05 and |log fold change| >0.5.
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Gene expression profiles GSE110147 were downloaded from the Gene Expression Omnibus database platform was GPL6244[HuGene-1_0-st] Affymetrix Human Gene 1.0 ST Array. This microarray obtained samples from recipients’ organs of 22 patients with IPF, 10 with NSIP, and 5 with mixed IPF-NSIP undergoing lung transplantation. Normal lung tissue (n=11) was obtained from tissue that flanks lung cancer resections. In this study, 22 lung samples from IPF were classified as the IPF group. Meanwhile, 11 normal lung samples were classified as the control group.
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Gene expression profiles GSE110147 were downloaded from the Gene Expression Omnibus database platform was GPL6244[HuGene-1_0-st] Affymetrix Human Gene 1.0 ST Array. This microarray obtained samples from recipients’ organs of 22 patients with IPF, 10 with NSIP, and 5 with mixed IPF-NSIP undergoing lung transplantation. Normal lung tissue (n=11) was obtained from tissue that flanks lung cancer resections. In this study, 22 lung samples from IPF were classified as the IPF group. Meanwhile, 11 normal lung samples were classified as the control group.
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A total of 9,183 DEGs were identified, of which 4,545 genes were down-regulated, and 4638 were up-regulated.
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A total of 9,183 DEGs were identified, of which 4,545 genes were down-regulated, and 4638 were up-regulated.
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Gene expression profiles GSE110147 were downloaded from the Gene Expression Omnibus database platform was GPL6244[HuGene-1_0-st] Affymetrix Human Gene 1.0 ST Array. This microarray obtained samples from recipients’ organs of 22 patients with IPF, 10 with NSIP, and 5 with mixed IPF-NSIP undergoing lung transplantation. Normal lung tissue (n=11) was obtained from tissue that flanks lung cancer resections. In this study, 22 lung samples from IPF were classified as the IPF group. Meanwhile, 11 normal lung samples were classified as the control group.
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{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:34734011", "kind": "science-record", "revision": 4, "content_hash": "sha256:c7330ac0ccf19eee446179c41439c621511fdb3c65c5b9198d2de0ba88cb2a80", "created_at": "2026-11-01T17:36:24Z", "updated_at": "2026-11-01T22:05:04Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Bioinformatic analysis of differentially expressed genes and pathways in idiopathic pulmonary fibrosis.", "doi": "10.21037/atm-21-4224", "pmid": "34734011", "authors": ["Nana Li", "Lingxiao Qiu", "Cheng Zeng", "Zeming Fang", "Shanshan Chen", "Xiangjin Song", "Heng Song", "Guojun Zhang"], "journal": "Annals of translational medicine", "year": 2021, "abstract": "BACKGROUND: Using bioinformatic methods to explore the differentially expressed genes (DEGs) of human idiopathic pulmonary fibrosis (IPF) and to elucidate the pathogenesis of IPF from the genetic level.\nMETHODS: The GSE110147 gene expression profile was downloaded from the GEO database. The data of lung adenocarcinoma (LUAD) samples, lung squamous cell carcinoma (LUSC) samples and normal samples were downloaded from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. DEGs between IPF patients and healthy donors were analyzed using the GEO2R tool. Use the \"clusterprofiler\" package in R software to perform gene ontology (GO) and KEGG pathway enrichment analysis, and then perform function annotation and protein-protein interaction (PPI) network construction in the STRING online tool. The Genome Browser tool of the university of california santa cruz (UCSC) online website was used to predict transcription factors (TFs) of genes. In the final, the results were analyzed synthetically.\nRESULTS: A total of 9,183 DEGs were identified, of which 4,545 genes were down-regulated, and 4638 were up-regulated. MMP1, SPP1, and BPIFB1 were the top three DEGs with the highest significant up-regulation. These DEGs played an important role in the occurrence of IPF through the MAPK (mitogen-activated protein kinase) signaling pathway. Furthermore, 50 DEGs were enriched in the expression of PD-L1 and the PD-1 checkpoint pathway in cancer, of which 11 genes were re-enriched in the pathway of non-small cell lung cancer. The expression of the 11 genes were extensively regulated by CTCFL, SP2 and ZNF341. Most of them were differentially expressed between lung cancers and normal lung tissues. The overall survival (OS) curve of LUAD were significantly stratified by AKT2, KRAS, PIK3R1, meanwhile the OS curve of LUAC was significantly stratified by MAPK3.\nCONCLUSIONS: Bioinformatics analysis revealed that DEGs including MPP1 might be potential targets and biomarkers of IPF, and the MAPK signaling pathway is related to the occurrence and development of IPF. The development of IPF lung cancer complications may be related to the activation of genes enriched in PD-L1 expression and PD-1 checkpoint pathway, which provides clues to the pathogenesis of IPF combined with lung cancer.", "claims": [{"id": "claim-method", "statement": "GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r) was used to detect differentially expressed genes (DEGs) of IPF compared to normal tissues. The screening condition was P<0.05 and |log fold change| >0.5.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:34734011", "locator": "sections[4] \"DEGs screening and data processing\" paragraph 2", "quote": "GEO2R (http://www.ncbi.nlm.nih.gov/geo/geo2r) was used to detect differentially expressed genes (DEGs) of IPF compared to normal tissues. 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