STAT3: An Anti-Invasive Factor in Colorectal Cancer?

Cancers

Petrus Rudolf de Jong²  Ji-Hun Mo¹  Alexandra R. Harris²  Jongdae Lee² 

[1] Department of Otorhinolaryngology, Dankook University College of Medicine, 16-5 Anseo-dong, Cheonan, Chungcheongnam-do 330-715, Korea; E-Mail:;Department of Medicine, University of California, San Diego, 9500 Gilman Dr. MC 0663, La Jolla, CA 92093, USA; E-Mails:

关键词: signal transducer and activator of transcription 3 (STAT3);    colorectal cancer (CRC);    metastasis;    epithelial to mesenchymal transition (EMT);    Snail-1 (SNAI-1);    glycogen synthase kinase 3β (GSK3β);    Snail;    adenomatous polyposis coli (APC);    tight junction (TJ);    matrix metalloproteinases (MMPs);   

DOI  :  10.3390/cancers6031394

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.