Significance of decoy receptor 3 (Dcr3) and external-signal regulated kinase 1/2 (Erk1/2) in gastric cancer

Yang, Dongyuan; Fan, Xueli; Yin, Ping; Wen, Qiang; Feng, Yan; Yuan, Sibo; Liu, Bin; Zhuang, Guohong; Liu, Zhongchen

doi:10.1186/1471-2172-13-28

Cited by 16 publications

(15 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results indicated that TIPE was expressed in the cytoplasm and nucleolus of GC cells, and that TIPE mRNA expression was significantly increased in GC compared with normal gastric tissues. The results were consistent with a previous finding that TIPE is overexpressed in human malignant tumors (8)(9)(10)14). However, no association was observed between TIPE mRNA expression and nodal status or differentiation in the present study.…”

supporting

confidence: 82%

See 1 more Smart Citation

Expression of tumor necrosis factor-α-induced protein 8 in stage III gastric cancer and the correlation with DcR3 and ERK1/2

Liu

Qiu

et al. 2016

Oncology Letters

Self Cite

View full text Add to dashboard Cite

Abstract. Tumor necrosis factor (TNF)-α-induced protein 8 (TIPE) is a recently identified protein that is considered to be associated with various malignancies, including esophageal, breast and pancreatic cancer; however, the importance of TIPE in gastric cancer (GC) remains unknown. Decoy receptor 3 (DcR3) is a member of the tumor necrosis factor receptor superfamily that is expressed in digestive system neoplasms. The expression of DcR3 is regulated by the mitogen-activated protein kinase (MAPK)/MAPK kinase/extracellular signal-regulated kinase (ERK) signaling pathway. Reverse transcription-polymerase chain reaction was performed to detect the expression of TIPE, ERK and DcR3 in the pathological and tumor-adjacent normal gastric tissues of 30 patients that demonstrated stage III gastric adenocarcinoma. The expression and distribution of the TIPE protein was examined using immunohistochemistry, and the clinical significance and expression levels of DcR3 and ERK1/2 were evaluated. The expression of TIPE, ERK1/2 and DcR3 in the tumor tissues of GC was significantly increased compared with paracarcinoma tissues (P<0.05). In addition, TIPE expression positively correlated with DcR3 and ERK1 levels (r= 0.538 and r=0.462, respectively; P<0.05). There was no statistical difference between tumor tissues from patients with varying age, gender, differentiation or lymph node metastasis (P>0.05). TIPE may be vital in the progression of GC. TIPE may be associated with the expression of DcR3 and ERK1/2, which may be involved in the cell apoptosis of GC. The present study elucidates the potential function of TIPE as a novel marker and therapeutic target for GC.

show abstract

supporting

confidence: 82%

“…The overexpression of DcR3 in tumor cells protects the cells from apoptosis (13). Therefore, DcR3 and ERK are vital in the development of GC (14).…”

Section: Introductionmentioning

confidence: 99%

Expression of tumor necrosis factor-α-induced protein 8 in stage III gastric cancer and the correlation with DcR3 and ERK1/2

Liu

Qiu

et al. 2016

Oncology Letters

Self Cite

View full text Add to dashboard Cite

show abstract

“…Cells were incubated with 25 ng/ml sFasL and/or 5 mg/ml IgG, 5 mg/ml rDcR3, 50 mM PD098059 for 24 h. (C) Phosphorylation of ERK1/2 was analyzed by Western blot. Cells were incubated with 25 ng/ml sFasL and/or 5 mg/ml IgG, 5 mg/ml rDcR3, 50 uM PD098059 for 24 h. [34,35]. We found that DcR3 promoted ERK1/2 phosphorylation, but did not affect the Akt pathway.…”

Section: Tl1aedr3 and Lightelymphotoxin B Receptor Interactionsmentioning

confidence: 98%

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

Zhang

Zhao

et al. 2015

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

“…DcR3 has been found to be highly expressed in many malignant tumors 20–23. Silencing of DcR3 can affect the proliferation, invasion, and metastasis ability of tumor cells and sensitize tumor cells to Fas-mediated apoptosis 24,25.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of DcR3 sensitizes hepatocellular carcinoma cells to TRAIL-induced apoptosis

Liang¹,

Yang²,

Li³

et al. 2017

OTT

View full text Add to dashboard Cite

Decoy receptor 3 (DcR3) has been recently described as an antiapoptosis and prometastasis factor since it can competitively bind to FasL, TL1A, and LIGHT, and it is highly expressed in many malignant tumors. Downregulation of DcR3 can promote tumor cell apoptosis and inhibit metastasis. A previous study demonstrated that reduction of DcR3 could induce tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in pancreatic cancer cells. However, whether such an effect is seen in hepatocellular carcinoma (HCC) remains to be explored. This study was designed to investigate the sensitivity of HCC cells to TRAIL after silencing DcR3, and this was done by evaluating the expression of DcR3 in HCC cells and the effect on TRAIL-mediated apoptosis after downregulation of DcR3. Our data showed that DcR3 was highly expressed in HepG2, BEL-7402, Hep3B, Huh-7, MHCC97H, and SMCC7721 cell lines compared with normal liver cell line LO-2. Both HepG2 and BEL-7402 were tolerant to TRAIL-mediated apoptosis, and the tolerance was negatively correlated to the expression of DcR3. Silencing of DcR3 with shRNA and treatment with TRAIL induced obvious apoptosis in HepG2 and BEL-7402, with more cancer cells found in the G1 phase. SiDcR3 combined with TRAIL could induce activation of caspases-3, -8, and -9, raise the expression of the apoptotic protein Bax, and reduce the expression of antiapoptotic proteins (Bcl-2, Mcl-1, Bcl-XL, IAP-2, and survivin). Caspase-8 inhibitor Ac-IETD-CHO significantly decreased the activation of caspase cascade, indicating that the extrinsic pathway may have a vital role in the apoptotic events induced by SiDcR3/TRAIL. Furthermore, our results showed that the TRAIL death receptor 5 (DR5) was upregulated and that DR5 neutralizing antibody abrogated the effect of SiDcR3. Our results demonstrated that downregulation of DcR3 could enhance TRAIL-mediated apoptosis in HCC through the death receptor pathway. In the future, this might be useful as a clinical treatment method of liver cancer.

show abstract

Significance of decoy receptor 3 (Dcr3) and external-signal regulated kinase 1/2 (Erk1/2) in gastric cancer

Cited by 16 publications

References 18 publications

Expression of tumor necrosis factor-α-induced protein 8 in stage III gastric cancer and the correlation with DcR3 and ERK1/2

Expression of tumor necrosis factor-α-induced protein 8 in stage III gastric cancer and the correlation with DcR3 and ERK1/2

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

Downregulation of DcR3 sensitizes hepatocellular carcinoma cells to TRAIL-induced apoptosis

Contact Info

Product

Resources

About