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• W2034126710 abstract "Interleukin-4 (IL-4)-induced Stat6 activities (phenotypes) vary among human cancer cells, of which the HT-29 cell line carries an active Stat6high phenotype, while Caco-2 carries a defective Stat6null phenotype, respectively. Cancer cells with Stat6high show resistance to apoptosis and exaggerated metastasis, suggesting the clinical significance of Stat6 phenotypes. We previously showed that Stat6high HT-29 cells exhibited low constitutive expression of Stat6-negative regulators SOCS-1 and SHP-1 because of gene hypermethylation. This study further examined the constitutive expression of other closely related SOCS family numbers including SOCS-3, SOCS-5, SOCS-7, and CISH using RT-PCR. Similar to SOCS-1 and SHP-1, Stat6high HT-29 cells expressed low constitutive mRNA of SOCS-3, SOCS-7, and CISH than Stat6null Caco-2 cells. Interestingly, DNA demethylation using 5-aza-2′-deoxycytidine in HT-29 cells up-regulated mRNA expression of the above genes, indicating a hypermethylation status, which was confirmed by methylation-specific sequencing in selected SOCS-3 gene. Furthermore, defective Stat6null Caco-2 exhibited impaired phosphorylation of Stat6 after IL-4 stimulation by flow cytometry, in keeping with the notion of an over-performed negative regulation. The findings that IL-4/Stat6 phenotypes show differential expression of multiple negative regulators suggest a model that a collective force of powerful negative regulators, directly and indirectly, acts on Stat6 activation, which may result in differential Stat6 phenotypes." @default.
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• W2034126710 date "2009-12-01" @default.
• W2034126710 modified "2023-10-03" @default.
• W2034126710 title "Defective Interleukin-4/Stat6 Activity Correlates With Increased Constitutive Expression of Negative Regulators<i>SOCS-3</i>,<i>SOCS-7</i>, and<i>CISH</i>in Colon Cancer Cells" @default.
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• W2034126710 doi "https://doi.org/10.1089/jir.2009.0004" @default.
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