Wnt/-catenin signaling is required for crypt structure maintenance. We previously observed nuclear accumulation of Ser-552 phosphorylated -catenin (p-Cat Ser-552 ) in intestinal epithelial cells (IEC) during colitis and colitis-associated cancer. Data here delineate a novel multiprotein cytosolic complex (MCC) involved in -catenin signaling in the intestine. The MCC contains p85␣, the class IA subunit of PI3K, along with -catenin, 14-3-3, Akt, and p110␣. MCC levels in IEC increase in colitis and colitis-associated cancer patients. IEC-specific p85␣-deficient (p85 ⌬IEC ) mice develop more severe dextran sodium sulfate colitis due to delayed ulcer healing and reduced epithelial -catenin activation. In colonic IEC, p85␣ deficiency did not alter PI3K signaling. In vitro shRNA depletion of individual complex members disrupts the MCC and reduces -catenin signaling. Despite worse colitis, p85 ⌬IEC mice have reduced tumor burden after azoxymethane/dextran sodium sulfate treatment. Together the data indicate that the -catenin MCC is needed for mucosal repair and carcinogenesis. This novel MCC may be an attractive therapeutic target in preventing cancer in colitis patients.
We report a case of E. histolytica, which is a rare parasitic infection in North America. A 66-year-old Ecuadorian female had an intermittent six-month history of bloating, explosive diarrhea and significant abdominal distension. Histopathological specimen obtained via colonoscopy revealed colitis due to E. histolytica. Diagnosis is best accomplished by the combination of serology or antigen testing together with identification of the parasite in the stool or extra-intestinal sites or histologic examination when necessary. With medical tourism and an increase of immigrants from South and Central America, disease endemic to those areas should always be considered.
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