(p38 MAPKs) function in a wide variety,of
signaling pathways. However, the role of p38s is cell type- and stimulus-dependent. The present study aimed to evaluate the effects of p38 MAPK inhibitor on human colon cancer cells.\n\nMethodology: The effect of p38 MAPK inhibitor, FR167653, on DLD-1 and selleck chemical SW480 was investigated related to cell proliferation, apoptosis induction and caspase activity. Additionally, the effect of FR167653 on colon cancer cell migration, MMPs production and ability to adhere to extracellular matrix was investigated.\n\nResults: Inhibitor of p38 MAPK dose-dependently suppressed the proliferative activity of both cell lines, and increased the induction of cell apoptosis. The caspase-3, 8, and 9 activities were
accompanied in the pathway. Neither cell migration, MMPs production, nor the ability to adhere extracellular matrix were affected by FR167653.\n\nConclusions: Inhibitor of p38 MAPK suppressed the proliferation of colon cancer cells by induction of cell apoptosis selleck chemicals llc through the caspase activation. The present results suggest the pro-oncogenic role of p38 in colon cancer, and its inhibition would be a novel strategy for the prevention and treatment of colon cancer.”
“Histopathologic differentiation between the stages of Barrett’s carcinogenesis is often challenging. Liver-intestine (LI)-cadherin, an intestine-specific marker, is involved in intestinal metaplasia development in gastric and colon cancers and could be of value in diagnosis and differentiation.\n\nTo examine the expression of LI-cadherin in the sequence of Barrett’s carcinogenesis and to evaluate its association with clinicopathological data.\n\nLI-cadherin expression was immunohistologically investigated, by use of anti-CDH17 antibody, in gastric mucosa (GM) biopsies taken from the cardia (n = 9), in Barrett’s esophagus (BE) without intraepithelial neoplasia (without IEN) (n = 9) and BE with low-grade IEN (n = 11), and in esophageal adenocarcinoma (ADC) (n = 13).\n\nThe
immunoreactivity score was highest in adenocarcinoma (mean IRS = 4.0), and dropped gradually from BE with IEN and BE without IEN (mean IRS = 2.0) to cardia mucosa (IRS = 0). Similarly, the intensity Selleck MI-503 of staining and the percentage of positive cells increased during the sequential stages of BE carcinogenesis. Comparative analysis showed that LI-cadherin expression was significantly different between cardiac epithelium and ADC. Also, percentage of positive cells in GM was significantly different from that in BE with IEN. LI-cadherin IRS was lower for tumors with poor differentiation than for moderately differentiated tumors, but the difference was not statistically significant.\n\nLI-cadherin is a sensitive marker of intestinal metaplasia and can be helpful for early histologic diagnosis of Barrett’s esophagus; it is, however, not significantly different between BE with and without IEN, and cannot be used to distinguish between these.