The detection of EBP50 expression using quantum dot immunohistochemistry in pancreatic cancer tissue and down-regulated EBP50 effect on PC-2 cells

Ji, Mengyao; Fan, Dikun; Lv, Xin; Peng, Xiulan; Lei, Xiaofei; Dong, Weiguo

doi:10.1007/s10735-012-9424-0

Cited by 12 publications

(14 citation statements)

References 34 publications

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“…EBP50 has been indicated to be a tumor suppressor in several types of tumor ( 10 ). Previous studies conducted by the authors of the present study have demonstrated that the downregulation of EBP50 expression promotes the growth of gastric and pancreatic cancer cells ( 12 , 13 ), and that the overexpression of EBP50 regulates the apoptosis of pancreatic cancer cells by decreasing the expression levels of Bcl-2 ( 11 ).…”

Section: Introductionsupporting

confidence: 52%

EBP50 inhibits pancreatic cancer cell growth and invasion by targeting the β-catenin/E-cadherin pathway

Fan²,

Liu

et al. 2015

Experimental and Therapeutic Medicine

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Ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) has previously been demonstrated to be associated with the malignant transformation of numerous types of human cancer. The aim of the present study was to investigate the effect of EBP50 overexpression on pancreatic cancer and the underlying mechanism. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of EBP50 in human pancreatic cancer tissue specimens. Furthermore, pBK-CMV-HA-EBP50 and the pBK-CMV-HA vectors were transfected into pancreatic cancer cells and the effect of EBP50 upregulation on the proliferation and invasion of the cells was investigated. In addition, the effect of EBP50 overexpression on β-catenin and E-cadherin expression was evaluated. The results revealed that overexpression of EBP50 suppressed cell growth and invasion in two human pancreatic cancer cell lines. Overexpression of EBP50 also suppressed β-catenin expression and increased E-cadherin expression. Thus, the present study demonstrated that EBP50 inhibits pancreatic cancer cell growth and invasion through targeting the β-catenin/E-cadherin pathway. The results suggest that EBP50 may function as a potential tumor suppressor and thus may serve as a potential therapeutic target.

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Section: Introductionsupporting

confidence: 52%

EBP50 inhibits pancreatic cancer cell growth and invasion by targeting the β-catenin/E-cadherin pathway

Fan²,

Liu

et al. 2015

Experimental and Therapeutic Medicine

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“…A previous study reported that the downregulation of EBP50 promoted PC cell proliferation, increased the colony-forming ability of cells and accelerated G1-to-S phase progression (16). In the present study, EBP50 overexpression significantly induced growth inhibition, G1-to-S cell cycle arrest and cell apoptosis in two PC cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…The cells were collected after 24 or 48 h. Transfection with Pbk-CMV-HA was used as the negative control (17). The stably transfected cell lines were constructed using a previously described method (16). Cells were trypsinized and reseeded into a 12-well plate.…”

Section: Methodsmentioning

confidence: 99%

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EBP50 regulates the apoptosis of pancreatic cancer cells by decreasing the expression levels of Bcl-2

Liu²,

et al. 2014

Experimental and Therapeutic Medicine

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Increasing evidence has demonstrated that ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) is involved in the malignant transformation of numerous human cancers. The present study investigated the involvement of EBP50 overexpression in the tumorigenicity of pancreatic cancer (PC). The results revealed that overexpression of EBP50 suppressed cell growth, promoted cell apoptosis and arrested G1-to-S phase progression in two human PC cell lines. Overexpression of EBP50 also suppressed B-cell lymphoma 2 (Bcl-2) expression. Furthermore, nude mouse tumor xenograft models were established by the subcutaneous injection of cell lines stably transfected with an EBP50-expressing plasmid. The in vivo data indicated that overexpression of EBP50 inhibited the growth of the PC tumors and induced cell apoptosis. Thus, the present study demonstrated that EBP50 overexpression induces growth inhibition and apoptosis in PC by decreasing Bcl-2 expression. The results suggest that EBP50 may function as a potential tumor suppressor in vivo and in vitro.

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“…It was reported that NHERF1 is significantly downregulated in multiple cancers, including colorectal cancer (9), particularly in early carcinogenesis (21), cervical (27), pancreatic cancer (28) and high-grade glioblastoma (14). Recently, NHERF1 is regarded as a new marker in colorectal cancer (9).…”

Section: Discussionmentioning

confidence: 99%

Wnt signaling pathway upregulates DNMT1 to trigger NHERF1 promoter hypermethylation in colon cancer

Guo¹,

Wang²,

Jia³

et al. 2018

Oncol Rep

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NHERF1 is downregulated and has been identified as a new marker of colorectal cancer. However, the molecular mechanism of NHERF1 downregulation in colon cancer is not well understood. In the present study, we demonstrated that the NHERF1 mRNA level was downregulated and correlated with outcomes in colon cancer patients. NHERF1 expression was associated with EMT phenotype. High levels of promoter methylation of NHERF1 in colon cancer were observed. NHERF1 expression was restored by demethylation treatment. In addition, a negative correlation between methylation and mRNA expression of NHERF1 was observed in the TCGA dataset. Moreover, DNMT1 inhibited NHERF1 expression in vivo. DNMT1 expression was found to be negatively correlated with NHERF1 and NHERF1 expression was also restored by a DNMT1 inhibitor. DNMT1 and NHERF1 were regulated by the Wnt signaling pathway. In addition, among DNMT1 high expression patients, the Wnt signaling pathway was negatively correlated with NHERF1 expression. In contrast, among DNMT1 low expression patients, the Wnt signaling pathway was not correlated with NHERF1 expression. In conclusion, Wnt signaling increases DNMT1 expression. DNMT1 contributes to promoter hypermethylation and epigenetic NHERF1 silencing in colon cancer. In addition, we provide novel insight into the mechanisms underlying the regulation of NHERF1 expression and occurrence/progression of colon cancer.

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The detection of EBP50 expression using quantum dot immunohistochemistry in pancreatic cancer tissue and down-regulated EBP50 effect on PC-2 cells

Cited by 12 publications

References 34 publications

EBP50 inhibits pancreatic cancer cell growth and invasion by targeting the β-catenin/E-cadherin pathway

EBP50 inhibits pancreatic cancer cell growth and invasion by targeting the β-catenin/E-cadherin pathway

EBP50 regulates the apoptosis of pancreatic cancer cells by decreasing the expression levels of Bcl-2

Wnt signaling pathway upregulates DNMT1 to trigger NHERF1 promoter hypermethylation in colon cancer

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