Journal
CANCERS
Volume 6, Issue 3, Pages 1394-1407Publisher
MDPI
DOI: 10.3390/cancers6031394
Keywords
signal transducer and activator of transcription 3 (STAT3); colorectal cancer (CRC); metastasis; epithelial to mesenchymal transition (EMT); Snail-1 (SNAI-1); glycogen synthase kinase 3 beta (GSK3 beta); Snail; adenomatous polyposis coli (APC); tight junction (TJ); matrix metalloproteinases (MMPs)
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Funding
- Crohn's and Colitis Foundation of America (CCFA)
- NIH [AI095623]
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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.
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