Soluble Fas ligand released by colon adenocarcinoma cells induces host lymphocyte apoptosis: an active mode of immune evasion in colon cancer

Song, Eunseok; Chen, J; Ouyang, N; Su, Fengxi; Wang, M; Heemann, Uwe

doi:10.1038/sj.bjc.6692042

Cited by 14 publications

(7 citation statements)

References 29 publications

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“…For immunohistochemistry [ 36 ], the samples were incubated with an integrin β3 antibody at 4°C overnight. The sections were then treated with a secondary antibody, followed by further incubation with a streptavidin-horseradish peroxidase complex.…”

Section: Methodsmentioning

confidence: 99%

MiR-320a acts as a prognostic factor and Inhibits metastasis of salivary adenoid cystic carcinoma by targeting ITGB3

et al. 2015

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BackgroundSalivary Adenoid cystic carcinoma (SACC) patients with local invasion and lung metastasis are often resistant to conventional therapy such as operation, chemotherapy and radiotherapy. To explore the underling mechanisms, we studied the roles of miRNA in regulating invasiveness of SACC cells.MethodsMicroRNA profiling was done in SACC cells with microarray. MiRNA mimics or antisense oligonucleotide was transfected and invasiveness of SACC cells was evaluated by adhesion assay and transwell assay. The target gene of miRNA was identified by luciferase reporter assay and “rescue” experiment. Tumor metastasis was evaluated by BALB/c-nu mice xenografts. MiRNA and its target gene expression were identified by in-situ hybridization and immunohistochemistry respectively, in 302 patients from affiliated hospitals of Sun Yat-sen University and in 148 patients from affiliated hospitals of Central South University, and correlated to the clinicopathological status of the patients.ResultsMiR-320a was down-regulated in high lung metastatic ACCM and SACC-LM cells compared with the corresponding low metastatic ACC2 and SACC-83 cells, and inhibited adhesion, invasion and migration of SACC cells by targeting integrin beta 3 (ITGB3). In vivo, enforced miR-320a expression suppressed metastasis of SACC xenografts. In the two independent sets, miR-320a was downregulated in primary SACCs with metastasis compared to those without metastasis, and low expression of this miRNA predicts poor patient survival and rapid metastasis. Multivariate analysis showed that miR-320a expression was an independent indicator of lung metastasis.ConclusionsMiR-320a inhibits metastasis in SACCs by targeting ITGB3 and may serve as a therapeutic target and prognostic marker in salivary cancers.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-015-0344-y) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

MiR-320a acts as a prognostic factor and Inhibits metastasis of salivary adenoid cystic carcinoma by targeting ITGB3

et al. 2015

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“… 143 By targeting these two ligases, ceramide might enhance the efficacy of Fas ligand-based CRC therapy, particularly cytotoxic T-lymphocyte-based immunotherapy. 145 …”

Section: Ring-type E3 Ligases As Therapeutic Targetsmentioning

confidence: 99%

Functional significance and therapeutic implication of ring-type E3 ligases in colorectal cancer

et al. 2017

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Accumulative studies revealed that E3 ubiquitin ligases have important roles in colorectal carcinogenesis. The pathogenic mechanisms of colorectal cancer (CRC) initiation and progression are complex and heterogeneous, involving somatic mutations, abnormal gene fusion, deletion or amplification and epigenetic alteration, which may cause aberrant expression or altered function of E3 ligases in CRC. Defects of E3 ligases have been reported to be involved in the molecular etiology and pathogenesis of CRC. The aberrant expressed E3 ligases can function as either oncogenes or tumor suppressors depending on ubiquiting target substrates in CRC. Recently, considerable progress has been made in our understanding of the potential roles of E3 ligase-mediated ubiquitylation in colorectal carcinogenesis. There are mainly two subtypes of E3 ubiquitin ligases in humans, as defined by the presence of either a HECT domain or a RING finger domain on the basis of structural similitude. Most cancer-associated E3 ligases participate in regulating the cell cycle, apoptosis, gene transcription, cell signaling and DNA repair, the critical parts of CRC tumorigenesis. In this review, we have provided a comprehensive summary of abnormally expressed E3 ligases and their related pivotal mechanistic effects in CRC. In particular, we have highlighted the function of RING-type E3 ubiquitin enzymes in modulating cancer signaling pathways, immunity and tumor microenvironment in CRC development and progression; their mechanism(s) of action in CRC involving both ubiquitylation-dependent and ubiquitylation-independent effects; and the potential of RING E3 ligases as molecular biomarkers for predicting patient prognosis and as therapeutic targets in CRC. A better understanding of E3 ligase-mediated substrates' ubiquitylation involved in the development of CRC will provide new insights into the pathophysiology mechanisms of CRC, and unravel novel prognostic markers and therapeutic strategies for CRC.

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“…38 Similarly, sFasL shed from colon adenocarcinoma cells elicited apoptosis of Fas-expressing Jurkat cells. 39 However, other studies have shown that the cytotoxic activity of sFasL may be lacking or less potent. 40 , 41 sFasL may also act as a negative regulator that limits Fas-mediated cell death by competing with mFasL for Fas binding.…”

Section: Discussionmentioning

confidence: 99%

Early septic insult in neonatal pigs increases serum and urinary soluble Fas ligand and decreases kidney function without inducing significant renal apoptosis

Soni

Adebiyi

2016

Renal Failure

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Apoptosis of renal tubular and glomerular cells during kidney disease involves activation of Fas ligand (FasL)-dependent death pathway. The significance of FasL in neonates with septic acute kidney injury (AKI) is unresolved, but an increase in renal FasL production, and/or infiltration of circulating FasL into the kidneys may occur following initial septic insult. Here, we examined whether soluble Fas ligand (sFasL) levels are altered during early phase of septic AKI in neonates. Six hours of polymicrobial sepsis elicited by cecal ligation and puncture (CLP) elevated serum C-reactive protein (CRP) (a bacteremia and sepsis marker) concentration in anesthetized and mechanically ventilated neonatal pigs. Serum creatinine and urea nitrogen concentrations were increased by ∼39% and 46%, respectively, following 6 h of CLP in the pigs. The urinary level of NGAL, an early marker of AKI was also elevated by ∼71% in the septic pigs. The basal concentration of sFasL in the serum and urine of neonatal pigs was similar. Six hours of CLP significantly increased serum and urine sFasL levels in the pigs by ∼24% and 68%, respectively. However, there was no evidence of caspase activation to suggest an induction of cellular apoptotic process in the kidneys of the septic pigs. These findings suggest that an increase in circulating and urinary sFasL during early septic AKI in neonatal pigs is not associated with renal apoptosis.

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Soluble Fas ligand released by colon adenocarcinoma cells induces host lymphocyte apoptosis: an active mode of immune evasion in colon cancer

Cited by 14 publications

References 29 publications

MiR-320a acts as a prognostic factor and Inhibits metastasis of salivary adenoid cystic carcinoma by targeting ITGB3

MiR-320a acts as a prognostic factor and Inhibits metastasis of salivary adenoid cystic carcinoma by targeting ITGB3

Functional significance and therapeutic implication of ring-type E3 ligases in colorectal cancer

Early septic insult in neonatal pigs increases serum and urinary soluble Fas ligand and decreases kidney function without inducing significant renal apoptosis

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