MRGBP as a potential biomarker for the malignancy of pancreatic ductal adenocarcinoma

Ding, Feng; Zhang, Shuang; Gao, Shicheng; Shang, Jian; Li, Yanxia; Cui, Ning; Zhao, Qiu

doi:10.18632/oncotarget.19451

Cited by 12 publications

(20 citation statements)

References 35 publications

(39 reference statements)

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“…It has been demonstrated that MRGBP involves in regulation of a number of cellular processes such as replication, apoptosis, growth, and invasiveness . Similarly, our previous study has shown that MRGBP modulates PanCa cells proliferation, migration, and invasion …”

Section: Introductionsupporting

confidence: 58%

“…In our previous study, MRGBP expression was confirmed to be significantly upregulated and be related to poor prognosis in PanCa. What's more, we also found downregulation of MRGBP inhibits proliferation, migration and invasion, but causes apoptosis in PanCa.…”

Section: Resultsmentioning

confidence: 83%

“…The molecular mechanism of PanCa is highly heterogeneous that is accompanied by various genetic abnormal expressions. Therefore, to overcome this global challenging problem, our previous study had for the first time identified that MRGBP would be a useful biomarker and predict poor prognosis in PanCa . However, why MRGBP is highly expressed in PanCa have puzzled us in the past.…”

Section: Discussionmentioning

confidence: 99%

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RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

Ding

Zhang

Gao

et al. 2018

J of Cellular Biochemistry

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miRNAs are small noncoding RNAs that act as critical epigenetic regulators in tumor carcinogenesis. In this study, our data showed that miR-137 was significantly downregulated in 58 pairs of human pancreatic cancer (PanCa) tissues and PanCa cell lines. Furthermore, the deregulated miR-137 was correlated with increased tumor size, higher TNM stage, and worse prognosis in pancreatic cancer. Functional studies demonstrated that overexpression of miR-137 dramatically suppressed cell proliferation and induced cell apoptosis in vitro. Meanwhile, upregulated miR-137 remarkably inhibited migration and invasion of pancreatic cancer cells. Further studies indicated that MRGBP was identified as the direct downstream target gene of miR-137. In addition, MRGBP expression is significantly downregulated in miR-137-transfected cells. Our previous study revealed that silencing of MRGBP suppressed the growth of PanCa cells in vitro and in vivo and also promoted apoptosis, and inhibited migration and invasion of PanCa cells, which are consistent with the effects of miR-137 overexpression. Taken together, our findings suggest that miR-137 may function as a novel tumor promoter through directly targeting MRGBP in PanCa.

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Section: Introductionsupporting

confidence: 58%

Section: Resultsmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

Ding

Zhang

Gao

et al. 2018

J of Cellular Biochemistry

Self Cite

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“…Furthermore, they revealed that MRGBP siRNA knockdown could reduce tumor growth in vivo, suggesting that MRGBP could be the potential therapeutic targets for cutaneous squamous cell carcinoma. In addition, upregulated expression of MRGBP was also observed in pancreatic ductal adenocarcinoma, prostate cancer and cervical cancer cells(35)(36)(37). All these studies suggested that MRGBP functioned as an oncogene that could promote the tumorigenesis.…”

mentioning

confidence: 84%

Systematic analyses of regulatory variants in DNase I hypersensitive sites identified two novel lung cancer susceptibility loci

Dai

Amos

et al. 2019

Carcinogenesis

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DNase I hypersensitive sites (DHS) are abundant in regulatory elements, such as promoter, enhancer and transcription factor binding sites. Many studies have revealed that disease-associated variants were concentrated in DHS-related regions. However, limited studies are available on the roles of DHS-related variants in lung cancer. In this study, we performed a large-scale case–control study with 20 871 lung cancer cases and 15 971 controls to evaluate the associations between regulatory genetic variants in DHS and lung cancer susceptibility. The expression quantitative trait loci (eQTL) analysis and pathway-enrichment analysis were performed to identify the possible target genes and pathways. In addition, we performed motif-based analysis to explore the lung-cancer-related motifs using sequence kernel association test. Two novel variants, rs186332 in 20q13.3 (C>T, odds ratio [OR] = 1.17, 95% confidence interval [95% CI]: 1.10–1.24, P = 8.45 × 10−7) and rs4839323 in 1p13.2 (T>C, OR = 0.92, 95% CI: 0.89–0.95, P = 1.02 × 10−6) showed significant association with lung cancer risk. The eQTL analysis suggested that these two SNPs might regulate the expression of MRGBP and SLC16A1, respectively. What’s more, the expression of both MRGBP and SLC16A1 was aberrantly elevated in lung tumor tissues. The motif-based analysis identified 10 motifs related to the risk of lung cancer (P < 1.71 × 10−4). Our findings suggested that variants in DHS might modify lung cancer susceptibility through regulating the expression of surrounding genes. This study provided us a deeper insight into the roles of DHS-related genetic variants for lung cancer.

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“…These E/M hybrid cells possess a higher metastatic risk and a gene signature composed by both24 epithelial and mesenchymal genes leading to a poor outcome (5, 9, 33). PDAC exhibit E/M hybrid cells (8, 22, 24, 34) that may contribute to the well-known heterogeneity in this kind of tumour. The role of E/M hybrid cells on PDAC aggressiveness remains largely unknown but they should impact cancer cell invasion and dissemination (8).…”

Section: Discussionmentioning

confidence: 99%

E-cadherin is a structuring component of invadopodia in pancreatic cancer

Dobric

Germain

Bonier

et al. 2020

Preprint

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Invasion/metastasis axis is the major driver of cancer mortality. By maintaining tissue cohesion, E-cadherin is considered as a protective marker for tumoral progression. However, recent studies suggested that the appearance of hybrid epithelial-mesenchymal (E/M) cells still expressing E-cadherin is favourable for the establishment of metastasis. This hypothesis is consistent with the observation that most pancreatic ductal adenocarcinomas (PDAC) are invasive and express E-cadherin in primary tumour and metastases. By using a data constituted by a series of patient-derived xenografts (PDX) from the PaCaOmics multi-centric clinical trial, we show that E-cadherin expression is not associated with stages of the pathology, prognosis, and overall survival in PDAC. The role of E-cadherin in PDAC aggressiveness was tested both in vitro and in cancer cell implantation models. We show that E-cadherin is a key component of membrane protrusions implicated in the extracellular matrix remodelling and degradation, called invadopodia. E-cadherin downregulation in a pancreatic model of E/M hybrid cells reveals that E-cadherin downregulates Arp2/3 complex expression. As this complex is essential for branched actin structure, E-cadherin depletion strongly impaired invadopodia formation. On the other hand, we demonstrate that E-cadherin interacts with the membrane protease MT1-MMP at the in-vadopodial membrane. E-cadherin could be recycled back to the invadopodial membrane simultaneously with MT1-MMP. Indeed, both Rab7 vesicle-dependant and/or a Rab11 vesicle-dependant pathway are required for both E-cadherin and MT1-MMP trafficking. This new localization of E-cadherin and its implication in cell invasion shines a new light on hybrid EMT features in tumoral invasion.

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MRGBP as a potential biomarker for the malignancy of pancreatic ductal adenocarcinoma

Cited by 12 publications

References 35 publications

RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

RETRACTED: MiR‐137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP

Systematic analyses of regulatory variants in DNase I hypersensitive sites identified two novel lung cancer susceptibility loci

E-cadherin is a structuring component of invadopodia in pancreatic cancer

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