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Crosstalk of Sp1 and Stat3 signaling in pancreatic cancer pathogenesis

期刊

CYTOKINE & GROWTH FACTOR REVIEWS
卷 23, 期 1-2, 页码 25-35

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.cytogfr.2012.01.003

关键词

Therapy; Angiogenesis; Metastasis

资金

  1. National Cancer Institute, National Institutes of Health [R01-CA129956, R01-CA148954, R01CA152309]
  2. National Natural Science Foundation of China [81101844]

向作者/读者索取更多资源

Pancreatic cancer progression is attributed to genetic and epigenetic alterations and a chaotic tumor microenvironment. Those diverse upstream signal factors appear to converge on specific sets of central nuclear regulators, namely, transcription factors. Specificity Protein 1 (Sp1) and signal transducer and activator of transcription 3 (Stat3) are central transcription factors that regulate a number of pathways important to tumorigenesis, including tumor cell-cycle progression, apoptosis, angiogenesis, metastasis, and evasion of the immune system. Recently, researchers demonstrated many types of crosstalk of Sp1 and Stat3 in tumor signal transduction and that these factors function cooperatively to activate targeted genes and promote tumorigenesis in pancreatic cancer. Therefore, targeting both Sp1 and Stat3 is a potential preventive and therapeutic strategy for pancreatic cancer. (C) 2012 Elsevier Ltd. All rights reserved.

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