1994
DOI: 10.1002/ijc.2910570314
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Expression of APO‐1 (CD95), a member of the NGF/TNF receptor superfamily, in normal and neoplastic colon epithelium

Abstract: APO-1 is a 48-kDa cell-membrane protein identical to the Fas antigen now designated CD95. It is a member of the NGF/TNF receptor superfamily. Anti-APO-1 monoclonal antibody induces apoptosis in a variety of cell types expressing this antigen. We immunohistochemically investigated APO-1 expression in normal colon mucosa, 20 adenomas, 258 colon carcinomas and 10 liver metastases and carried out in vitro studies using a panel of colon-carcinoma cell lines. Immunohistochemically, APO-1 was regularly expressed at t… Show more

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Cited by 276 publications
(227 citation statements)
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“…Bosentan alone dose-dependently increased apoptosis in SW480 cells, while it had little effect on HT29 cells (Figure 4, open symbols). In the presence of FasL, HT29 cells were partially resistant to FasL-mediated apoptosis after 24 h of treatment, while SW480 cells were sensitive to FasL-induced apoptosis (Figure 4, closed symbols), confirming previous information for SW480 cells (Möller et al, 1994 Two ET-receptor antagonists structurally unrelated to bosentan, BQ123 (ET A -specific) and BQ788 (ET B -specific), were investigated. Both BQ123 or BQ788 (at 80 mM concentrations) alone or in combination significantly ( Figure 4C; Po0.0004 for all treatments vs control), but not synergistically, sensitised HT29 cells to FasLmediated apoptosis like bosentan.…”
Section: Bosentan Sensitises Human Colon Carcinoma Cell To Fasl-inducsupporting
confidence: 85%
“…Bosentan alone dose-dependently increased apoptosis in SW480 cells, while it had little effect on HT29 cells (Figure 4, open symbols). In the presence of FasL, HT29 cells were partially resistant to FasL-mediated apoptosis after 24 h of treatment, while SW480 cells were sensitive to FasL-induced apoptosis (Figure 4, closed symbols), confirming previous information for SW480 cells (Möller et al, 1994 Two ET-receptor antagonists structurally unrelated to bosentan, BQ123 (ET A -specific) and BQ788 (ET B -specific), were investigated. Both BQ123 or BQ788 (at 80 mM concentrations) alone or in combination significantly ( Figure 4C; Po0.0004 for all treatments vs control), but not synergistically, sensitised HT29 cells to FasLmediated apoptosis like bosentan.…”
Section: Bosentan Sensitises Human Colon Carcinoma Cell To Fasl-inducsupporting
confidence: 85%
“…Fas protein is expressed in variable levels on the surface of several colon cancer cell lines. In some cell lines, low expression of Fas may be up-regulated by the cytokines TNF-a or interferon gamma (IFN-y) to levels similar to that of activated T cells (Yonehara et al, 1989;Itoh et al, 1991;Moller et al, 1994 (Yonehara et al, 1989;Abreu-Martin et al, 1995), while growth of KM12C cells is inhibited by the anti-Fas antibody (Owen-Schaub et al, 1993, 1994. Metastatic variants of KM12C cells are more resistant to the effects of the antibody, despite a similar level of Fas expression (Owen-Schaub et al, 1994).…”
Section: Discussionmentioning
confidence: 99%
“…Fas signalling has also been linked to apoptosis outside the lymphoid population, including the regression of ovarian follicles after ovulation and maintenance of cellular homeostasis in the liver (Adachi et al, 1995;Hakuno et al, 1996). The epithelial layer of the normal colonic mucosa expresses Fas protein at high levels, from the bottoms of the crypts to the luminal surface (Leithauser et al, 1993;Moller et al, 1994). A functional role for Fas receptors in the colon has not yet been demonstrated, as the Fas ligand has not been detected in the colon, except in subsets of lymphocytes in the lamina propria .…”
mentioning
confidence: 99%
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“…11,12 One of the strategies that tumor cells have developed to escape NKG2D-mediated cytolysis by NK cells or cells expressing NKG2D is down-regulating NKG2D ligands such as MICA, 13,14 a process also called shedding. Tumor cells also escape Fas-mediated apoptosis by decreasing surface expression of Fas, 15,16 secreting an antagonistic 'decoy' receptor, 17 expressing anti-apoptotic molecules such as BCL2 family members, 17,18 down-regulating and mutating pro-apoptotic genes such as BAX, APAF1 or Fas. [19][20][21][22][23] In our earlier study 24 we combined the function of NKG2D-mediated cytolysis and Fas-mediated apoptosis into one functional fusion protein by using the extracellular domain of MULT1 and the transmembrane and intracellular domains of Fas in a mouse model.…”
Section: Introductionmentioning
confidence: 99%