Literature DB >> 27035208

PageRank analysis reveals topologically expressed genes correspond to psoriasis and their functions are associated with apoptosis resistance.

Xue Zeng1, Jingjing Zhao2, Xiaohong Wu1, Hongbo Shi2, Wali Liu1, Bingnan Cui1, Li Yang3, Xu Ding1, Ping Song1.   

Abstract

Psoriasis is an inflammatory skin disease. Deceleration in keratinocyte apoptosis is the most significant pathological change observed in psoriasis. To detect a meaningful correlation between the genes and gene functions associated with the mechanism underlying psoriasis, 927 differentially expressed genes (DEGs) were identified using the Gene Expression Omnibus database, GSE13355 [false discovery rate (FDR) <0.01; |log fold change >1] with the package in R langue. The selected DEGs were further constructed using the search tool for the retrieval of interacting genes, in order to analyze the interaction network between the DEGs. Subsequent to PageRank analysis, 14 topological hub genes were identified, and the functions and pathways in the hub genes network were analyzed. The top‑ranked hub gene, estrogen receptor‑1 (ESR1) is downregulated in psoriasis, exhibited binding sites enriched with genes possessing anti‑apoptotic functions. The ESR1 gene encodes estrogen receptor α (ERα); a reduced level of ERα expression provides a crucial foundation in response to the anti‑apoptotic activity of psoriatic keratinocytes by activating the expression of anti‑apoptotic genes. Furthermore, it was detected that the pathway that is associated most significantly with psoriasis is the pathways in cancer. Pathways in cancer may protect psoriatic cells from apoptosis by inhibition of ESR1 expression. The present study provides support towards the investigation of ESR1 gene function and elucidates that the interaction with anti‑apoptotic genes is involved in the underlying biological mechanisms of resistance to apoptosis in psoriasis. However, further investigation is required to confirm the present results.

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Year:  2016        PMID: 27035208     DOI: 10.3892/mmr.2016.4999

Source DB:  PubMed          Journal:  Mol Med Rep        ISSN: 1791-2997            Impact factor:   2.952


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  6 in total

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