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World J Gastroenterol. Aug 14, 2014; 20(30): 10279-10287
Published online Aug 14, 2014. doi: 10.3748/wjg.v20.i30.10279
Published online Aug 14, 2014. doi: 10.3748/wjg.v20.i30.10279
STAT3 and sphingosine-1-phosphate in inflammation-associated colorectal cancer
Andrew V Nguyen, Department of Biological Sciences and Geology, Queensborough-CUNY, Bayside, NY 10461, United States
Yuan-Yuan Wu, Department of Pathology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10461, United States
Elaine Y Lin, Department of Medicine, Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, NY 10461, United States
Author contributions: All authors contributed to the manuscript.
Correspondence to: Elaine Y Lin, PhD, Assistant Professor, Department of Medicine, Einstein Cancer Center, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, United States. elaine.lin@einstein.yu.edu
Telephone: +1-718-4303138
Received: November 20, 2013
Revised: March 2, 2014
Accepted: April 15, 2014
Published online: August 14, 2014
Revised: March 2, 2014
Accepted: April 15, 2014
Published online: August 14, 2014
Core Tip
Core tip: Patients with inflammatory bowel diseases have a predisposition for the development of colorectal cancer (CRC). We summarize current literature on the interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3) inflammatory pathway and its association with CRC. Recent papers within the last couple of years have demonstrated the crosstalk between IL-6, STAT3 and sphingosine-1-phosphate pathways in inflammation associated tumorigenesis in intestine. This signaling cascade in tumor cells appears to be an essential pathway for CRC tumor progression. Current therapies exploiting sphingolipid signaling have provided an attractive strategy against inflammation-associated CRC.