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• W2023561138 startingPage "1058" @default.
• W2023561138 abstract "Abstract In this study, we demonstrated that STAT3, a well-characterized transcription factor expressed in continuously activated oncogenic form in the large spectrum of cancer types, induces in malignant T lymphocytes the expression of DNMT1, the key effector of epigenetic gene silencing. STAT3 binds in vitro to 2 STAT3 SIE/GAS-binding sites identified in promoter 1 and enhancer 1 of the DNMT1 gene. STAT3 also binds to the promoter 1 region and induces its activity in vivo. Treatment of the malignant T lymphocytes with STAT3 siRNA abrogates expression of DNMT1, inhibits cell growth, and induces programmed cell death. In turn, inhibition of DNMT1 by a small molecule inhibitor, 5-aza-2-deoxy-cytidine, and 2 DNMT1 antisense DNA oligonucleotides inhibits the phosphorylation of STAT3. These data indicate that STAT3 may in part transform cells by fostering epigenetic silencing of tumor-suppressor genes. They also indicate that by inducing DNMT1, STAT3 facilitates its own persistent activation in malignant T cells. Finally, these data provide further rationale for therapeutically targeting STAT3 in T-cell lymphomas and, possibly, other malignancies." @default.
• W2023561138 created "2016-06-24" @default.
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• W2023561138 date "2006-08-01" @default.
• W2023561138 modified "2023-10-06" @default.
• W2023561138 title "STAT3 induces transcription of the DNA methyltransferase 1 gene (DNMT1) in malignant T lymphocytes" @default.
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• W2023561138 doi "https://doi.org/10.1182/blood-2005-08-007377" @default.
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