IndraLab
Statements
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"Besides, upstream activators of Stat3, such as IL-6 and Src, also promote the activation of Jab1 and COPS5 transcription and translation through interacting with Stat3."
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"We further investigated whether an upstream activator of Stat3, the cytokine IL-6, could be driving increased Jab1 expression."
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"In turn, the oncogenic transcription factor STAT3 positively regulates JAB1 expression, indicative of a positive feedback loop."
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"We also identify a region whereby CCAAT and enhancer binding protein-beta (C/EBP-beta), signal transducer and activator of transcription-3 (Stat3), and GATA1 induce Jab1 transcription and identify a potential upstream oncogenic signaling molecule that may be key to the regulation of Jab1 expression in cancer."
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"Treatment with the cytokine IL-6 resulted in increased Jab1 expression that was blocked by inhibition of Stat3."
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"Interestingly, reactivation of Stat3 in normal mammary epithelial cells (MCF-10A, MCF-10F) is sufficient to reactivate Jab1 expression."
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"Because Stat3 expression in NPC was associated with Jab1 expression, we sought to determine whether the overexpression of Stat3 could enhance Jab1 transcription in NPC cells."
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"Our studies also revealed that Stat3 functions by binding to Jab1 and COPS5 promoter, promotes its activity and increases Jab1 and COPS5 transcription."
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"In summary, the present study demonstrates that the Src and Stat3 and C/EBP signaling pathways positively regulate the expression of the Jab1 oncogene."
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"Our previous studies demonstrated that Stat3 [XREF_BIBR] and non coding RNAs [XREF_BIBR] contribute to overexpression of Jab1 and COPS5 in cancer, and highly expressed Jab1 and COPS5 regulates DNA damage response, which confers chemotherapy and radiotherapy resistance to tumor cells [XREF_BIBR]."
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"STAT3 knockdown reduces JAB1 promoter activity, JAB1 mRNA, and JAB1 protein expression levels."