The relevance of apoptosis for cellular homeostasis and tumorigenesis: APOPTOSIS AND INTESTINAL TUMORIGENESIS Part 2

Apoptosis in intestinal tumorigenesis: What is the evidence that abnormalities in apoptosis are involved in the development of intestinal tumours? Using morphology to quantify apoptosis, a number of studies have found an increased apoptosis index from normal colonic epithelium through adenomas to the carcinoma stage. Additional evidence comes from the observation that a number of dietary factors (eg, fibre) and chemopreventive agents (eg, nonsteroidal anti-inflammatory ([NSAIDs]) prevent colonic tumour formation by promoting apoptosis. For example, it has been proposed that the chemopreven-tive effect of NSAIDs results from increased intestinal apoptosis brought about by decreased expression of Bcl-2 as a result of cyclo-oxygenase (COX)-2 inhibition. Shop online to always get enjoying safe and quick shopping.

A further role of apoptosis in intestinal tumorigenesis may lie at the epithelial-lymphoid cell interface. Fas ligand (FasL) induces apoptosis in sensitive immunocytes (Fas receptor [FasR]/APO-1/CD95 receptor positive) and regulates several immune responses, including contributing to immune privilege. FasL was originally thought to be expressed only in lymphoid cells but has now been shown to be expressed in epithelial cells from many organs. This has been termed the ‘Fas counter-attack’. FasL expression has been demonstrated in a number of human colon cancer cell lines in vitro and neoplastic colon epithelial cells in vivo, suggesting that the Fas counter-attack is a prevalent mechanism of immune evasion in colonic cancers.

 

Category: Gastroenterology

Tags: Apoptosis, bcl-2 family, Gastrointestinal cancer, Intestinal crypt, p53, Stem cell