Crosstalk of Sp1 and Stat3 signaling in pancreatic cancer pathogenesis.

作者: Chen Huang , Keping Xie

DOI: 10.1016/J.CYTOGFR.2012.01.003

关键词:

摘要: Pancreatic cancer progression is attributed to genetic and epigenetic alterations a chaotic tumor microenvironment. Those diverse "upstream signal" factors appear converge on specific sets of central nuclear regulators, namely, transcription factors. Specificity Protein 1 (Sp1) signal transducer activator 3 (Stat3) are that regulate number pathways important tumorigenesis, including cell-cycle progression, apoptosis, angiogenesis, metastasis, evasion the immune system. Recently, researchers demonstrated many types crosstalk Sp1 Stat3 in transduction these function cooperatively activate targeted genes promote tumorigenesis pancreatic cancer. Therefore, targeting both potential preventive therapeutic strategy for

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