PRL-3 and E-cadherin show mutual interactions and participate in lymph node metastasis formation in gastric cancer

Pryczynicz, Anna; Guzińska‐Ustymowicz, Katarzyna; Niewiarowska, Katarzyna; Cepowicz, Dariusz; Kemonä, A

doi:10.1007/s13277-014-1855-7

Cited by 11 publications

(10 citation statements)

References 23 publications

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“…E-cadherin methylation rate was much lower than expected, while it was correlated with lymph node metastasis in RGC tumors, which recapitulates the previous reports [38]. Moreover, E-cadherin hypermethylation is observed in IN-IB in contrast to IN-IM or RN.…”

Section: Discussionsupporting

confidence: 89%

Prediction of onset of remnant gastric cancer by promoter DNA methylation of CDO1/HOPX/Reprimo/E-cadherin

et al. 2019

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Background Early detection of remnant gastric cancer (RGC) is required to reduce the risk of death, but long-term endoscopic surveillance is difficult after gastrectomy. In this study, data for the methylation status of 4 methylation genes ( CDO1, HOPX, Reprimo, and E-cadherin ) to predict the onset of RGC are presented. Results The 4 genes showed hypermethylation in RGC tumors in contrast to the corresponding non-cancerous mucosa tissues. The methylation level in the non-cancerous mucosa tissues of the initial surgery was obviously high in initial malignant disease for CDO1 ( P = 0.0001), while in initial benign one for E-cadherin ( P = 0.003). Promoter DNA methylation status in the remnant non-cancerous mucosa tissues together with the basic clinical data in turn predicted either initial malignant disease or initial benign disease with a high AUC score of 0.94, suggesting that methylation events are differentially recognized between the initial malignant and benign disease. We then finally confirmed that 4 genes hypermethylation of the non-cancerous tissues by biopsy prior to onset of RGC could predict terms until RGC occurred ( P < 0.0001). Methods A total of 58 RGC patients were used to establish the model. The 4 genes promoter methylation were analyzed for DNA obtained from the patient’s specimens using quantitative methylation specific polymerase chain reaction. Conclusions This risk model would help provide guidance for endoscopic surveillance plan of RGC after gastrectomy.

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Section: Discussionsupporting

confidence: 89%

Prediction of onset of remnant gastric cancer by promoter DNA methylation of CDO1/HOPX/Reprimo/E-cadherin

et al. 2019

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“…PRL‐3 expression had been found to be associated with metastasis in many types of tumors . In the present study, we found that patients with high‐level expression of PRL‐3 have a high risk of lung metastasis.…”

Section: Discussionsupporting

confidence: 61%

“…PRL‐3, also known as PTP4A3, belongs to the family of tyrosine phosphatases, which play a fundamental role in regulating protein phosphorylation balance . PRL‐3 expression has been evaluated in various human cancers, and it was found to be associated with invasion, metastasis, and poor prognosis . Wang et al.…”

Section: Discussionmentioning

confidence: 99%

“…PRL‐3, which belongs to the phosphatase of regenerating liver (PRL) family, was first found to be highly expressed in liver metastases of patients with colorectal cancer . Until now, much literature had suggested that high expression of PRL‐3 was considered to be associated with a poor prognosis in many types of malignant tumors , including acute myeloid leukemia , gastric cancer , ovarian cancer , and hepatocellular cancer . PRL‐3 had been found to be involved in the following biological function: cytoskeleton rebuilding ; the regulation of cell adhesion to promote invasion and metastasis of cancer cells ; the activation of the Rho family and MMP‐2 to stimulate the invasion and motility of cancer cells ; tumor growth through the mechanism of epithelial–mesenchymal transformation (EMT) mediated by the AKT, PI3K, and STAT pathways .…”

Section: Introductionmentioning

confidence: 99%

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PRL‐3 promotes migration and invasion and is associated with poor prognosis in salivary adenoid cystic carcinoma

Dong

Ding

Chang

et al. 2015

J Oral Pathology Medicine

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Background PRL‐3 had been found to be involved in tumorigenesis in various malignancies. In this study, we investigated the role of PRL‐3 in the development, migration, and invasion of salivary adenoid cystic carcinoma (SACC).MethodsImmunohistochemistry (IHC) was used to analyze the role of PRL‐3 in the development and prognosis of SACC. Then, we overexpressed or inhibited the expression of PRL‐3 in paired SACC cells to analyze the role of PRL‐3 in the migration and invasion of SACC. In vitro migration and invasion assays were used. Western blotting was used to detect metastasis‐related protein levels.Results IHC results confirmed that the deregulation of PRL‐3 was a frequent event in SACC; the upregulation of PRL‐3 was related to clinical stages, vital status, and distant metastasis, which was associated with reduced overall survival and disease‐free survival. SACC‐LM cells with higher migratory and invasive abilities had more robust PRL‐3 protein expression than SACC‐83 cells with lower migratory and invasive abilities. PRL‐3 overexpression promoted cell migration, invasion, and proliferation, led to simultaneous upregulation of phosphorylated PRL‐3, pERK1/2, Slug, vimentin, and downregulation of E‐cadherin in SACC‐83 cells. However, the inhibition of PRL‐3 by PRL‐3 inhibitor or PRL‐3 siRNA in SACC‐LM cells inhibited cell migration, invasion, and proliferation, resulted in simultaneous downregulation of phosphorylated PRL‐3, pERK1/2, Slug, vimentin, and upregulation of E‐cadherin.ConclusionsOur results confirm that PRL‐3 plays an important role in the development of SACC and contributes to the migratory and invasive abilities of SACC.

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“…In recent years, an increasing number of reports have implicated PRL-3 as an activator of pathways involved in proliferation, invasion, and cell motility, such as phosphatidylinositol-3 kinase (PI3K)/serine threonine protein kinase AKT [12], the tyrosine protein kinase Src [13], Rho GTPases family [10], mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) kinase (MEK) [14], and epidermal growth factor receptor (EGFR) signaling [15], as well as mediating epithelial mesenchymal transition (EMT) by down-regulating phosphatase and tensin homolog (PTEN) [16] or the cadherin family [17,18]. Interestingly, PRL-3 can also recruit endothelial cells participating in tumor angiogenesis, an essential event for cancer progression [19].…”

Section: Introductionmentioning

confidence: 99%

Regulatory mechanisms of phosphatase of regenerating liver (PRL)-3

Rubio

Köhn

2016

Biochemical Society Transactions

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The phosphatase of regenerating liver (PRL)-3 is overexpressed in many human cancer types and tumor metastases when compared with healthy tissues. Different pathways and mechanisms have been suggested to modulate PRL-3 expression levels and activity, giving some valuable insights but still leaving an incomplete picture. Investigating these mechanisms could provide new targets for therapeutic drug development. Here, we present an updated overview and summarize recent findings concerning the different PRL-3 expression regulatory mechanisms and posttranslational modifications suggested to modulate the activity, localization, or stability of this phosphatase.

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PRL-3 and E-cadherin show mutual interactions and participate in lymph node metastasis formation in gastric cancer

Cited by 11 publications

References 23 publications

Prediction of onset of remnant gastric cancer by promoter DNA methylation of CDO1/HOPX/Reprimo/E-cadherin

Prediction of onset of remnant gastric cancer by promoter DNA methylation of CDO1/HOPX/Reprimo/E-cadherin

PRL‐3 promotes migration and invasion and is associated with poor prognosis in salivary adenoid cystic carcinoma

Regulatory mechanisms of phosphatase of regenerating liver (PRL)-3

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