Colorectal cancer (CRC) constitutes a significant portion of mortality and morbidity due to cancer around the world. The present study was designed to evaluate the possible effects of the JAK/STAT, TNF-alpha, and NF kappa B pathways, and the caspase-3 apoptoticmarker in human colorectal tissue. Data from tumor tissue and adjacent normal colon tissue (n:12) were obtained. Given the biological role of the JAK/STAT signaling pathway in human colorectal tissue, we evaluated interactions with TNF alpha, NF kappa B, and caspase-3. We measured the mRNA levels of STAT1, TNF-alpha, TNF-alpha R1A, NF kappa B, and caspase-3 by RT-PCR. The STAT1, TNF-alpha, TNF-alpha R1A, and NF kappa B mRNA levels were increased in colorectal cancer tissue compared to adjacent normal colon tissue (P < 0.01, P < 0.05, P < 0.05, and P < 0.05, respectively). There were no significant differences between colorectal cancer and adjacent normal colon tissue regarding the caspase-3 mRNA levels. STAT1 contributes to oncogenesis by promoting the progression of the cell cycle and preventing cells from undergoing apoptosis. In addition, TNF-alpha has proangiogenic activity and increases the neovascularization of tumors. According to our results, the mRNA levels of STAT1 and TNF-alpha were significantly higher in cancer tissues, but the mRNA levels of the apoptotic genes caspase-3 and 9 were similar to those of the normal colon tissue, suggesting that STAT1 and TNF-alpha are important components in the progression of colorectal cancer. These data support the importance of the JAK/STAT signaling pathway in colorectal cancer and suggest targets for intervention. We will be investigating potentially related genes, pathways, and interactions in our future studies. (C) 2016 Elsevier Inc. All rights reserved.