Department of Medicine, University of California, San Diego, 9500 Gilman Dr. MC 0663, La Jolla, CA 92093, USA.
Department of Otorhinolaryngology, Dankook University College of Medicine, 16-5 Anseo-dong, Cheonan, Chungcheongnam-do 330-715, Korea.
Cancers (Basel). 2014 Jul 3;6(3):1394-407. doi: 10.3390/cancers6031394.
Signal Transducer and Activator of Transcription 3 (STAT3) is activated in a majority of cancers, and promotes tumorigenesis and even metastasis through transcriptional activation of its target genes. Recently, we discovered that STAT3 suppresses epithelial-to-mesenchymal transition (EMT) and thus metastasis in a mouse model of colorectal cancer (CRC), while it did not affect the overall tumor burden. Furthermore, we found that STAT3 in intestinal epithelial cells (IEC) suppresses EMT by regulating stability of an EMT inducer, SNAI-1 (Snail-1). Here, STAT3 functions as an adaptor rather than a transcription factor in the post-translational modification of SNAI-1. In this review, we discuss the unexpected and contradictory role of STAT3 in metastasis of CRC and its clinical implications.
信号转导子和转录激活子 3（STAT3）在大多数癌症中被激活，并通过其靶基因的转录激活促进肿瘤发生甚至转移。最近，我们发现 STAT3 在结直肠癌（CRC）的小鼠模型中抑制上皮间质转化（EMT）和转移，而不影响总体肿瘤负担。此外，我们发现肠上皮细胞（IEC）中的 STAT3 通过调节 EMT 诱导因子 SNAI-1（Snail-1）的稳定性来抑制 EMT。在这里，STAT3 在 SNAI-1 的翻译后修饰中充当衔接子而不是转录因子。在这篇综述中，我们讨论了 STAT3 在 CRC 转移中的意外和矛盾作用及其临床意义。
