Decoy receptor 3 suppresses FasL-induced apoptosis via ERK1/2 activation in pancreatic cancer cells

Zhang, Yi; Li, Dechun; Zhao, Xin; Song, Shiduo; Zhang, Lifeng; Zhu, Dongming; Chen, Xiaochen; Zhou, Jian

doi:10.1016/j.bbrc.2015.06.074

Cited by 16 publications

(19 citation statements)

References 30 publications

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“…The expression of DcR3 is regulated by the mitogen-activated protein kinase (MAPK)/MAPK kinase/extracellular signal-regulated kinase (ERK) signaling pathway. The expression of TNFA-induced protein 8, ERK1/2 and DcR3 in the tumor tissues of GC was significantly increased compared with paracarcinoma tissues and TNFA-induced protein 8 expression positively correlated with DcR3 and ERK1/2 levels, which may be involved in the cell apoptosis of gastric and pancreatic cancer [55,56].…”

Section: Tumor Necrosis Factor-related Decoy Receptorsmentioning

confidence: 94%

“…The level of DcR3 protein and ERK1/2 phosphorylation in pancreatic carcinoma cells is up-regulated and RNAi knockdown of DcR3 expression reduced resistance to FasL-induced apoptosis and elevated expression of caspase 3, 8 and 9 as well as reduced ERK1/2 phosphorylation [56]. Thus, DcR3/TNFRS-F6B enhances ERK1/2 phosphorylation and opposes FasL signaling in pancreatic cancer cells.…”

Section: Tumor Necrosis Factor-related Decoy Receptorsmentioning

confidence: 94%

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The role of the TNF receptors and apoptosis inducing ligands in tumor growth

Minchenko¹,

Tsymbal²,

Minchenko³

et al. 2016

Ukr.Biochem.J.

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Tumor necrosis factor (TNF) superfamily receptors and TNF apoptosis inducing ligands play an important role in the realization of TNF function and control tumor growth. The TNF-related pathways are controlled by endoplasmic reticulum stress signaling, which has a crucial role in the control of cell proliferation and tumor growth. Furthermore, the inhibition of IRE1 (inositol requiring enzyme-1), which is a central mediator of endoplasmic reticulum stress sand mainly responsible for cell proliferation and apoptosis, leads to suppression of tumor growth through specific changes in the expression of genes encoding transcription factors, tumor suppressors, angiogenesis and apoptosis related proteins, including TNF superfamily receptors and TNF apoptosis inducing ligands. Therefore, changes in the expression level of TNF-related genes encoding TNF superfamily receptors and apoptosis inducing ligands possibly reflect metabolic reprogramming of cancer cells upon inhibition of IRE1-mediated endoplasmic reticulum stress signaling and correlate with suppression of glioma cell proliferation.

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Section: Tumor Necrosis Factor-related Decoy Receptorsmentioning

confidence: 94%

Section: Tumor Necrosis Factor-related Decoy Receptorsmentioning

confidence: 94%

The role of the TNF receptors and apoptosis inducing ligands in tumor growth

Minchenko¹,

Tsymbal²,

Minchenko³

et al. 2016

Ukr.Biochem.J.

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“…The DcR3-specific siRNA can efficiently inhibit cell growth and induce apoptosis via attenuating ERK and AKT activation, and the apoptosis rate is increased to 1.85 and 3.93 folds at 72 and 96 h after transfection, respectively [71]. Similarly, knockdown of DcR3 in pancreatic Pata8988 cancer cells reduces ERK1/2 phosphorylation with elevated expression of caspases and increased susceptibility to FasL-induced apoptosis [72]. In addition to siRNA, downregulation of DcR3 by triptolide also triggers the apoptosis of pancreatic cancer cells [67].…”

Section: Functional Study Of Dcr3 In Vitro By Knockdown or Overexpresmentioning

confidence: 99%

Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions

Hsieh

Lin

2017

J Biomed Sci

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Decoy receptor 3 (DcR3), also known as tumor necrosis factor receptor (TNFR) superfamily member 6b (TNFRSF6B), is a soluble decoy receptor which can neutralize the biological functions of three members of tumor necrosis factor superfamily (TNFSF): Fas ligand (FasL), LIGHT, and TL1A. In addition to ‘decoy’ function, recombinant DcR3.Fc is able to modulate the activation and differentiation of dendritic cells (DCs) and macrophages via ‘non-decoy’ action. DcR3-treated DCs skew T cell differentiation into Th2 phenotype, while DcR3-treated macrophages behave M2 phenotype. DcR3 is upregulated in various cancer cells and several inflammatory tissues, and is regarded as a potential biomarker to predict inflammatory disease progression and cancer metastasis. However, whether DcR3 is a pathogenic factor or a suppressor to attenuate inflammatory reactions, has not been discussed comprehensively yet. Because mouse genome does not have DcR3, it is not feasible to investigate its physiological functions by gene-knockout approach. However, DcR3-mediated effects in vitro are determined via overexpressing DcR3 or addition of recombinant DcR3.Fc fusion protein. Moreover, CD68-driven DcR3 transgenic mice are used to investigate DcR3-mediated systemic effects in vivo. Upregulation of DcR3 during inflammatory reactions exerts negative-feedback to suppress inflammation, while tumor cells hijack DcR3 to prevent apoptosis and promote tumor growth and invasion. Thus, ‘switch-on’ of DcR3 expression may be feasible for the treatment of inflammatory diseases and enhance tissue repairing, while ‘switch-off’ of DcR3 expression can enhance tumor apoptosis and suppress tumor growth in vivo.

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“…Decoy receptor 3 (DcR3 or TNFRSF6B) is a soluble receptor belonging to the tumor necrosis factor receptor superfamily (TNFRSF) that binds competitively to other TNFSF members, such as Fas ligand (FasL/TNFSF6/CD95L), LIGHT (TNFSF14), and TNF‐like molecule 1A (TL1A/TNFSF15) . Upregulation of DcR3 was associated with poor prognosis in several malignancies due to its effect on angiogenesis and the proliferation, invasion, and metastasis of tumor cells . However, very few studies have explored the clinicopathological role of DcR3 in oral cancer.…”

Section: Introductionmentioning

confidence: 99%

“…6 Upregulation of DcR3 was associated with poor prognosis in several malignancies [7][8][9][10][11][12][13][14][15][16] due to its effect on angiogenesis and the proliferation, invasion, and metastasis of tumor cells. [7][8][9][17][18][19] However, very few studies have explored the clinicopathological role of DcR3 in oral cancer. Epidermal growth factor receptor (EGFR) is overexpressed in OSCC and is associated with poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

Anti‐oral cancer effects of triptolide by downregulation of DcR3 in vitro, in vivo, and in preclinical patient‐derived tumor xenograft model

et al. 2018

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Background Aberrant expression of decoy receptor 3 (DcR3) is considered to be a diagnostic and therapeutic target for human cancers. The aim of this study was to assess DcR3 as a target of the anticancer effects of triptolide (TPL) in preclinical patient‐derived tumor xenograft (PDTX) models of oral squamous cell carcinoma (OSCC). Methods The expression of DcR3 was evaluated through immunohistochemistry, and correlations were examined using clinical variables. The effects of TPL on the expression of DcR3 and cell proliferation were investigated in OSCC cell lines and in PDTX models. Results DcR3 overexpression was associated with overall survival and tumor size. TPL significantly decreased tumor growth. Moreover, TPL inhibited the expression of metastasis‐associated protein 1 (MTA1), a transcription factor for DcR3 in vivo, in vitro, and in PDTX models. Conclusion TPL appeared to exert anticancer effects by repressing DcR3 and MTA1 in vitro, in vivo, and in PDTX models.

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Decoy receptor 3 suppresses FasL-induced apoptosis via ERK1/2 activation in pancreatic cancer cells

Cited by 16 publications

References 30 publications

The role of the TNF receptors and apoptosis inducing ligands in tumor growth

The role of the TNF receptors and apoptosis inducing ligands in tumor growth

Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions

Anti‐oral cancer effects of triptolide by downregulation of DcR3 in vitro, in vivo, and in preclinical patient‐derived tumor xenograft model

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