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Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis

Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis
Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis
Background: endometriosis is a frequently occurring disease in women, which seriously affects their quality of life. However, its etiology and pathogenesis are still unclear.

Methods: to identify key genes/pathways involved in the pathogenesis of endometriosis, we recruited 3 raw microarray datasets (GSE11691, GSE7305, and GSE12768) from Gene Expression Omnibus database (GEO), which contain endometriosis tissues and normal endometrial tissues. We then performed in-depth bioinformatic analysis to determine differentially expressed genes (DEGs), followed by gene ontology (GO), Hallmark pathway enrichment and protein-protein interaction (PPI) network analysis. The findings were further validated by immunohistochemistry (IHC) staining in endometrial tissues from endometriosis or control patients.

Results: we identified 186 DEGs, of which 118 were up-regulated and 68 were down-regulated. The most enriched DEGs in GO functional analysis were mainly associated with cell adhesion, inflammatory response, and extracellular exosome. We found that epithelial-mesenchymal transition (EMT) ranked first in the Hallmark pathway enrichment. EMT may potentially be induced by inflammatory cytokines such as CXCL12. IHC confirmed the down-regulation of E-cadherin (CDH1) and up-regulation of CXCL12 in endometriosis tissues.

Conclusions: utilizing bioinformatics and patient samples, we provide evidence of EMT in endometriosis. Elucidating the role of EMT will improve the understanding of the molecular mechanisms involved in the development of endometriosis.
2045-2322
Chen, Meihong
541db434-40cc-4e2a-832c-bdf6df02a443
Zhou, Yilu
1878565d-39e6-467d-a027-7320bf4cdaf2
Xu, Hong
4fcd36e9-a7a8-4b2c-a15c-61e1925ffa54
Hill, Charlotte
6d1cfed3-11b1-48af-b171-b8726ab673eb
Ewing, Robert
022c5b04-da20-4e55-8088-44d0dc9935ae
He, Deming
3f27f2ff-9cbc-4a50-b3bf-982580942051
Zhang, Xiaoling
49f0a7bf-bab6-44fa-9c3e-bcecf5c324be
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e
Chen, Meihong
541db434-40cc-4e2a-832c-bdf6df02a443
Zhou, Yilu
1878565d-39e6-467d-a027-7320bf4cdaf2
Xu, Hong
4fcd36e9-a7a8-4b2c-a15c-61e1925ffa54
Hill, Charlotte
6d1cfed3-11b1-48af-b171-b8726ab673eb
Ewing, Robert
022c5b04-da20-4e55-8088-44d0dc9935ae
He, Deming
3f27f2ff-9cbc-4a50-b3bf-982580942051
Zhang, Xiaoling
49f0a7bf-bab6-44fa-9c3e-bcecf5c324be
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e

Chen, Meihong, Zhou, Yilu, Xu, Hong, Hill, Charlotte, Ewing, Robert, He, Deming, Zhang, Xiaoling and Wang, Yihua (2020) Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis. Scientific Reports. (In Press)

Record type: Article

Abstract

Background: endometriosis is a frequently occurring disease in women, which seriously affects their quality of life. However, its etiology and pathogenesis are still unclear.

Methods: to identify key genes/pathways involved in the pathogenesis of endometriosis, we recruited 3 raw microarray datasets (GSE11691, GSE7305, and GSE12768) from Gene Expression Omnibus database (GEO), which contain endometriosis tissues and normal endometrial tissues. We then performed in-depth bioinformatic analysis to determine differentially expressed genes (DEGs), followed by gene ontology (GO), Hallmark pathway enrichment and protein-protein interaction (PPI) network analysis. The findings were further validated by immunohistochemistry (IHC) staining in endometrial tissues from endometriosis or control patients.

Results: we identified 186 DEGs, of which 118 were up-regulated and 68 were down-regulated. The most enriched DEGs in GO functional analysis were mainly associated with cell adhesion, inflammatory response, and extracellular exosome. We found that epithelial-mesenchymal transition (EMT) ranked first in the Hallmark pathway enrichment. EMT may potentially be induced by inflammatory cytokines such as CXCL12. IHC confirmed the down-regulation of E-cadherin (CDH1) and up-regulation of CXCL12 in endometriosis tissues.

Conclusions: utilizing bioinformatics and patient samples, we provide evidence of EMT in endometriosis. Elucidating the role of EMT will improve the understanding of the molecular mechanisms involved in the development of endometriosis.

Text
Bioinformatic in endometriosis-R1-final - Accepted Manuscript
Available under License Creative Commons Attribution.
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Accepted/In Press date: 7 May 2020

Identifiers

Local EPrints ID: 440729
URI: http://eprints.soton.ac.uk/id/eprint/440729
ISSN: 2045-2322
PURE UUID: 46608a83-45d7-4c8e-a65a-fd92e8925d62
ORCID for Robert Ewing: ORCID iD orcid.org/0000-0001-6510-4001
ORCID for Yihua Wang: ORCID iD orcid.org/0000-0001-5561-0648

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Date deposited: 14 May 2020 16:32
Last modified: 07 Oct 2020 02:08

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