Project description:To identify the target gene of ΔNp63α, in osteosarcoma cells, we performed the global gene expression profiling in SaOS- 2 cells stably overexpressing the ΔNp63α gene (SaOS- 2-ΔNp63α). ΔNp63α target genes were identified by comparison with genes expressed from SaOS-2-EV transfected with an empty vector ( SaOS-2-EV).
Project description:To identify the target gene of M-NM-^TNp63M-NM-1, in osteosarcoma cells, we performed the global gene expression profiling in SaOS- 2 cells stably overexpressing the M-NM-^TNp63M-NM-1 gene (SaOS- 2-M-NM-^TNp63M-NM-1). M-NM-^TNp63M-NM-1 target genes were identified by comparison with genes expressed from SaOS-2-EV transfected with an empty vector ( SaOS-2-EV). Total RNA was extracted from SaOS- 2-M-NM-^TNp63M-NM-1 and SaOS-2-EV cells cultured in three independent replicates for each condition. Cy3-labeled cRNA was synthesized and hybridized to Agilent human 8 x 60K microarrays. Raw data, obtained after array image analysis were normalized and used to retrieve differentially expressed genes in M-NM-^TNp63M-NM-1 overexpressing SaOS- 2 cells and genes from control SaOS-2-EV cells.
Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.