Impact of FASL-induced apoptosis in the elimination of tumor cells by NK cells

Screpanti, Valentina; Wallin, Robert P. A.; Grandien, Alf; Ljunggren, Hans‐Gustaf

doi:10.1016/j.molimm.2004.07.033

Cited by 138 publications

(95 citation statements)

References 49 publications

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“…Although it has been proposed that the expression of Fas ligand (FasL) in tumors may play an important role in immune escape, apoptosis of tumor cells was induced by Fasmediated apoptotic signals through binding to the FasL of NK cells. NK cells kill virus-infected and tumor cells via several direct or indirect pathways (Liu et al, 1995;Kashii et al, 1999;Lieberman, 2003), including perforin/granzyme-and death receptor (FASL or TRAIL)-mediated cell death (Screpanti et al, 2005). We also observed that NDRG2-silenced SNU-620 cells were less susceptible than SNU-620-mock cells to death induced by activated human NK cells (data not shown).…”

Section: Discussionsupporting

confidence: 55%

Expression of NDRG2 is related to tumor progression and survival of gastric cancer patients through Fas-mediated cell death

Choi

Yoon²,

Park³

et al. 2007

Exp Mol Med

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Although N-myc downstream regulated gene 2 (NDRG2) has been known to be a tumor suppressor gene, the function of this gene has not been elucidated. In the present study, we investigated the expression and function of NDRG2 in human gastric cancer. Among seven gastric cancer and two non-cancer cell lines, only two gastric cancer cell lines, SNU-16 and SNU-620, expressed NDRG2, which was detected in the cytoplasm. Interestingly, NDRG2 was highly expressed in normal gastric tissues, but gastric cancer patients were divided into NDRG2-positive and -negative groups. The survival rate of NDRG2-negative patients was lower than that of NDRG2-positive patients. We confirmed that the loss of NDRG2 expression was a significant and independent prognostic indicator in gastric carcinomas by multivariate analysis. To investigate the role of NDRG2 in gastric cancer cells, we generated a NDRG2-silenced gastric cancer cell line, which stably expresses NDRG2 siRNA. NDRG2-silenced SNU-620 cells exhibited slightly increased proliferation and cisplatin resistance. In addition, inhibition of NDRG2 decreased Fas expression and Fas-mediated cell death. Taken together, these data suggest that inactivation of NDRG2 may elicit resistance against anticancer drug and Fas-mediated cell death. Furthermore, case studies of gastric cancer patients indicate that NDRG2 expression may be involved in tumor progression and overall survival of the patients.

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Section: Discussionsupporting

confidence: 55%

Expression of NDRG2 is related to tumor progression and survival of gastric cancer patients through Fas-mediated cell death

Choi

Yoon²,

Park³

et al. 2007

Exp Mol Med

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“…Both pathways require cell-to-cell contact and rely on surface receptors for activation (35). Several studies report death receptor-mediated tumor cell apoptosis by NK cells (36), and physiologic stress was shown to suppress FasL-mediated NK activity (37,38). Indeed, the current study showed that the expression of FasL on NK cells decreased following surgery and that our drug treatment counteracted this effect.…”

Section: Sectionmentioning

confidence: 47%

Improving Survival Rates in Two Models of Spontaneous Postoperative Metastasis in Mice by Combined Administration of a β-Adrenergic Antagonist and a Cyclooxygenase-2 Inhibitor

Glasner

Avraham

Rosenne

et al. 2010

The Journal of Immunology

213

177

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Clinical practice does not consider perioperative paracrine and neuroendocrine stress responses as risk factors for cancer recurrence, although recent animal studies provided supportive evidence. Suggested mechanisms include the effects of stress-hormones on tumor cells and on host physiology. In this study, in mice undergoing primary tumor excision, we tested the survival-enhancing potential of perioperative blockade of catecholamines and prostaglandins, and studied potential mediating mechanisms. C57BL/6J mice were inoculated intrafootpad with syngeneic B16F10.9-melanoma or Lewis lung carcinoma, and the paw was amputated when a developing tumor exceeded 100 μl. The clinically used β-adrenergic antagonist propranolol, and/or the cyclooxygenase-2 inhibitor etodolac, were administered once before amputation, and recurrence-free survival was monitored. In different studies, NK cytotoxicity, leukocytes' molecular functional markers, and vascular endothelial growth factor secretion by tumor cells were studied in the context of surgery and drug treatments. The findings indicated that the combination of propranolol and etodolac, but neither drug alone, significantly and markedly improved survival rates in both tumor models, and was as effective as established immunostimulatory agents (IL-12 and polyinosinic-polycytiylic acid). Surgery markedly reduced NK cytotoxicity and NK cell expression of Fas ligand and CD11a, reduced all circulating lymphocyte-subtype concentrations, and increased corticosterone levels. Propranolol and etodolac administration counteracted these perturbations. B16 and 3LL secreted vascular endothelial growth factor in vitro, but secretion was not affected by catecholamine agonists, prostaglandins, corticosterone, propranolol, or etodolac. Overall, propranolol and etodolac administration, which could be applied perioperatively in most cancer patients with minimal risk and low cost, has counteracted several immunologic and endocrinologic perturbations and improved recurrence-free survival rates in mice undergoing primary tumor excision.

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“…Following stimulation, NK cells release large amounts of immunostimulatory cytokines including IFN-g and TNF-a, and trigger target cell death through the perforin/granzyme pathway or extrinsic pathways of apoptosis (Fas/FasLigand or TRAIL) [7]. Expression of activating or inhibitory receptors on NK cells enables self and non-self recognition [8].…”

Section: Introductionmentioning

confidence: 99%

Human tumor‐induced and naturally occurring Treg cells differentially affect NK cells activated by either IL‐2 or target cells

et al. 2011

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Impact of FASL-induced apoptosis in the elimination of tumor cells by NK cells

Cited by 138 publications

References 49 publications

Expression of NDRG2 is related to tumor progression and survival of gastric cancer patients through Fas-mediated cell death

Expression of NDRG2 is related to tumor progression and survival of gastric cancer patients through Fas-mediated cell death

Improving Survival Rates in Two Models of Spontaneous Postoperative Metastasis in Mice by Combined Administration of a β-Adrenergic Antagonist and a Cyclooxygenase-2 Inhibitor

Human tumor‐induced and naturally occurring Treg cells differentially affect NK cells activated by either IL‐2 or target cells

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