Soluble Fas/APO-1 in tumor cells: a potential regulator of apoptosis?

Owen‐Schaub, Laurie B.; Angelo, Laura S.; Radinsky, Robert; Ware, Carl F.; Gesner, Thomas G.; Bartos, David

doi:10.1016/0304-3835(95)03834-j

Cited by 96 publications

(65 citation statements)

References 28 publications

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“…Cheng et a1 (8), however, recently reported the presence of elevated levels of sFas in sera from SLE patients, and they found that it exhibited inhibitory effects on Fas-dependent apoptosis in a mouse model of RA. On the other hand, recent studies by Owen-Schaub et al (17) and Weller et a1 (18) demonstrated sFas expression in anti-Fas-resistant tumor cell lines. It has been previously suggested that the deletion of sFas by TM may contribute to the resistance of anti-Fas MAb and the lack of apoptosis in human osteosarcoma cell lines.…”

Section: Discussionmentioning

confidence: 92%

Accumulation of soluble fas in inflamed joints of patients with rheumatoid arthritis

Hasunuma

Kayagaki

Asahara

et al. 1997

Arthritis & Rheumatism

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Objective. To examine the concentration of the soluble form of the Fas molecule (sFas) in the serum and synovial fluid of patients with rheumatoid arthritis (RA) and osteoarthritis (OA).Methods. The concentration of sFas in the serum of 15 normal subjects and in the synovial fluid and serum of 45 RA patients and 13 OA patients was determined. The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, and the level of several cytokines in serum and synovial fluid were also determined.Results. The synovial fluid concentration of sFas was higher in RA than in OA patients (P < 0.005). The Conclusion.Our data suggest that accumulation of sFas in the joint cavity of RA patients may inhibit apoptosis and exacerbate the inflammatory process.

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Section: Discussionmentioning

confidence: 92%

Accumulation of soluble fas in inflamed joints of patients with rheumatoid arthritis

Hasunuma

Kayagaki

Asahara

et al. 1997

Arthritis & Rheumatism

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“…Surface-associated immunoreactive Fas level did not change when cells were treated for 6 h with 1 or 4 mM sodium butyrate. Several tumor cell lines have been reported to produce and secrete soluble isoforms of the Fas receptor that can contribute to their Fas-resistance (Owen-Schaub et al, 1995a). These isoforms are able to inhibit the binding of Fas ligand or agonist anti-Fas antibodies to membraneassociated Fas.…”

Section: Resultsmentioning

confidence: 99%

Cancer cell sensitization to Fas-mediated apoptosis by sodium butyrate

et al. 1998

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Cancer cells often resist Fas-mediated apoptosis even when the Fas receptor is expressed at the cell surface. We show here that human and rat colon cancer cells undergo massive apoptosis when they are exposed to soluble Fas ligand in the presence of sodium butyrate, an agent that induces by itself only a low rate of apoptosis. Sodium butyrate potentiates Fasdependent apoptosis in seven out of eight colon cancer cell lines. Sodium butyrate does not increase Fas receptor cell surface expression and does not modify cell levels of Bcl-2, Bcl-x L , Bcl-x S and Bax. Sodium butyrate also induces tumor cell sensitization to the apoptotic effect of the combination of TNF-a and IFN-g, but it does not modify the level of the FADD/ Mort1 adaptator molecule, at the connection between Fas-and TNF-dependent apoptosis pathways. Because the clinical toxicity of butyrate is low, its ability to enhance Fas-signal delivery in cancer cells could be of therapeutic interest.

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“…CD95 receptor expression is widely distributed among tumors of various histological types; the susceptibility of cells to apoptosis induced by CD95 stimulation, however, is not correlated with the expression levels of this protein (Owen-Schaub et al, 1994). In accordance with these observations, the biological e ects of agonistic anti-CD95 (CH11) engagement di ered between the H1299 and DLD-1 cell lines expressing equivalent levels of cell surface CD95:anti-CD95 (CH11) caused apoptosis in H1299 cells, but not in DLD-1 cells.…”

Section: Discussionmentioning

confidence: 98%

Differential involvement of the CD95 (Fas/APO-1) receptor/ligand system on apoptosis induced by the wild-type p53 gene transfer in human cancer cells

et al. 1999

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The CD95 (Fas/APO-1) system regulates a number of physiological and pathological processes of cell death. The ligand for CD95 induces apoptosis in sensitive target cells by interacting with a transmembrane cell surface CD95 receptor. We previously reported that the recombinant adenovirus-mediated transfer of the wildtype p53 gene caused apoptotic cell death in a variety of human cancer cells. To better understand the mechanism responsible for this cell death signaling, we have investigated the potential involvement of the CD95 receptor/ligand system in p53-mediated apoptosis. The transient expression of the wild-type p53 gene upregulated the CD95 ligand mRNA as well as protein expression in H1299 human lung cancer cells de®cient for p53 and in DLD-1 and SW620 human colon cancer cells with mutated p53, all of which constitutively expressed CD95 receptor as shown by a¯ow cytometric analysis, and induced rapid apoptotic cell death as early as 24 h after gene transfer. However, the sensitivity to the cytolytic e ect of agonistic anti-CD95 antibody (CH11) varied among these cell lines: CH11 induced apoptosis in H1299 cells, but not in DLD-1 and SW620 cells despite their abundant CD95 receptor expression, suggesting that the CD95 receptors on DLD-1 and SW620 cells might be inactivated. In addition, an antagonistic anti-CD95 ligand antibody (4H9) that interfered with the CD95-receptor-ligand interaction partially reduced the apoptosis induced by the wild-type p53 gene transfer in H1299 cells, whereas apoptosis of DLD-1 and SW620 cells occurred in the presence of 4H9. Taken together, these ®ndings led us to conclude that the CD95 receptor/ligand system is di erentially involved in p53-mediated apoptosis, suggesting that the restoration of the wild-type p53 function may mediate apoptosis through CD95 receptor/ligand interactions as well as an alternative pathway.

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Soluble Fas/APO-1 in tumor cells: a potential regulator of apoptosis?

Cited by 96 publications

References 28 publications

Accumulation of soluble fas in inflamed joints of patients with rheumatoid arthritis

Accumulation of soluble fas in inflamed joints of patients with rheumatoid arthritis

Cancer cell sensitization to Fas-mediated apoptosis by sodium butyrate

Differential involvement of the CD95 (Fas/APO-1) receptor/ligand system on apoptosis induced by the wild-type p53 gene transfer in human cancer cells

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