Regulation of EMT by KLF4 in gastrointestinal cancer.
Regulation of EMT by KLF4 in gastrointestinal cancer.
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DOI：
10.2174/15680096113136660104
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发表时间：
2013-11
影响因子：
3
通讯作者：
Xie K
中科院分区：
文献类型：
--
作者：
Cui J;Shi M;Quan M;Xie K
胃肠道(GI)癌具有侵袭性的特点，但其潜在的机制尚不完全清楚。研究表明，上皮间充质转化(EMT)受一系列转录因子和信号通路的调控，与胃肠道癌细胞的增殖、侵袭和转移密切相关。从本质上讲，EMT是信号通路间串扰的产物。KRüppel-like factor4(KLF4)是一种锌指型转录因子，在大多数胃肠道肿瘤中表达降低或缺失。KLF4通过转录调控其下游靶基因，在胃肠道肿瘤的发生、增殖和分化中发挥重要作用。本文就KLF4与转化生长因子-β、Notch和Wnt信号通路的相互作用机制作一综述，并证明KLF4通过与转化生长因子-TRAN、Notch和Wnt信号通路的相互作用，负向调节GI癌的EMT。最后，我们指出了KLF4具有挑战性的新领域，这有助于更好地理解GI癌症侵袭性的机制。
Gastrointestinal (GI) cancer is characterized by its aggressiveness, but the underlying mechanism is not fully understood. Studies reveal that epithelial to mesenchymal transition (EMT), which is regulated by a series of transcription factors and signaling pathways, is strongly associated with GI cancer cell proliferation, invasion and metastasis. In essential, EMT is a product of crosstalk between signaling pathways. Krüppel-like factor 4 (KLF4), a zinc finger-type transcription factor, is decreased or lost in most GI cancers. By transcriptional regulating its downstream target genes, KLF4 plays important roles of GI cancer tumorigenesis, proliferation and differentiation. In this review, we focus on the mechanism of KLF4 in GI cancer EMT, and demonstrate that through crosstalk with TGF-β, Notch, and Wnt signaling pathways, KLF4 negatively regulates EMT of GI cancers. Finally, we indicate the challenging new frontiers for KLF4 which contributes to better understanding of the mechanism of GI cancer aggressiveness.
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作者：
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DOI：
10.1152/ajpgi.00203.2003
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