Ezrin protein overexpression predicts the poor prognosis of pancreatic ductal adenocarcinomas

Piao, Jinhua; Liu, Shusen; Xu, Yunjie; Wang, Changan; Lin, Zhenhua; Qin, Yunzhi

doi:10.1016/j.yexmp.2014.11.003

Cited by 38 publications

(38 citation statements)

References 25 publications

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“…EzR is a cytoplasmic peripheral membrane protein that functions as a substrate of protein tyrosine kinases, regulates cellular survival, adhesion, migration, and invasion. Importantly, EzR is also one of the key factors involved in tumor progression and metastasis in HCC (36)(37)(38)(39). Our finding supports the notion that KAL1 may function through tumor suppressor mechanisms and led us to speculate that KAL1 may interact with EzR and mediate tumorigenesis of HCC.…”

Section: Discussionsupporting

confidence: 84%

Translational implication of Kallmann syndrome-1 gene expression in hepatocellular carcinoma

Tanaka

Kanda

Sugimoto

et al. 2015

International Journal of Oncology

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Abstract. Accumulation of epigenetic alterations causes inactivation of tumor suppressors and contributes to the initiation and progression of hepatocellular carcinoma (HCC).Identification of methylated genes is necessary to improve our understanding of the pathogenesis of HCC and develop novel biomarkers and therapeutic targets. The Kallmann syndrome-1 (KAL1) gene encodes an extracellular matrixrelated protein with diverse oncological functions. However, the function of KAL1 in HCC has not been examined. We investigated the methylation status of the KAL1 promoter region in HCC cell lines, and evaluated KAL1 mRNA levels and those of genes encoding potential interacting cell adhesion factors. KAL1 mRNA expression level was heterogeneous in nine HCC cell lines, and reactivation of KAL1 mRNA expression was observed in cells with promoter hypermethylation of KAL1 gene after demethylation. In addition, KAL1 mRNA levels inversely correlated with those of ezrin in all nine HCC cell lines. KAL1 expression levels in 144 pairs of surgically-resected tissues were determined and correlated to clinicopathological parameters. KAL1 mRNA level was independent of the background liver status, whereas HCC tissues showed significantly lower KAL1 mRNA levels than corresponding noncancerous liver tissues. Downregulation of KAL1 mRNA in HCC was significantly associated with malignant phenotype characteristics, including elevated tumor markers, larger tumor size, vascular invasion, and hypermethylation of KAL1. Patients with downregulation of KAL1 were more likely to have a shorter overall survival than other patients, and multivariate analysis identified downregulation of KAL1 as an independent prognostic factor (hazard ratio 2.04, 95% confidence interval 1.11-3.90, P=0.022). Our results indicated that KAL1 may act as a putative tumor suppressor in HCC and is inactivated by promoter hypermethylation. KAL1 may serve as a biomarker of malignant phenotype of HCC.

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Section: Discussionsupporting

confidence: 84%

Translational implication of Kallmann syndrome-1 gene expression in hepatocellular carcinoma

Tanaka

Kanda

Sugimoto

et al. 2015

International Journal of Oncology

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“…Here, we show that ezrin expression is primarily down‐regulated in CCA, in contrast to the majority of clinical studies performed in other human carcinomas, in which ezrin expression has generally been shown to be increased . Our findings demonstrate that lack of or low expression of ezrin in CCA is associated with a more aggressive phenotype.…”

Section: Discussioncontrasting

confidence: 58%

Loss of ezrin in human intrahepatic cholangiocarcinoma is associated with ectopic expression of E‐cadherin

et al. 2016

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“…Increasing researches focus on the role of Ezrin in cancer invasion and metastasis since its initial identification. Overexpression of Ezrin is an independent prognostic factor with poor overall survival (OS) and disease-free survival (DFS) in pancreatic ductal adenocarcinomas [14], breast cancer [15] and oral squamous cell carcinoma (OSCC) [16], indicating the tumorpromotor function of Ezrin. Additionally, the expression and phosphorylation of Ezrin play a novel role in the apoptosis and proliferation of multiple human cancer cell lines [17][18][19].…”

Section: Original Papermentioning

confidence: 99%

Baicalein Inhibits Proliferation Activity of Human Colorectal Cancer Cells HCT116 Through Downregulation of Ezrin

Chen

Hou

Gao

et al. 2018

Cell Physiol Biochem

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Background/Aims: The present study was aimed at examining Ezrin expression in human colorectal cancer (CRC) tissues and elucidating the influence of baicalein on the proliferation of HCT116 cells. Methods: The expression of Ezrin was determined by qRT-PCR and immunohistochemistry. HCT116 cells were divided into four groups－ baicalein groups with various concentrations, pcDNA3.1-Ezrin group, si-Ezrin group and dual inhibitory group (baicalein + si-Ezrin). CCK-8 assay and flow cytometry (FCM) were employed to assess cell proliferation and to detect the distribution of cell cycle respectively. The expression levels of Ezrin protein and cell cycle-associated proteins were detected by using western blot. The proliferation ability of CRC cells was also evaluated in vivo. Results: Ezrin expression in CRC tissues was observably higher than that in adjacent colorectal tissues. With drug concentration and action time of baicalein increasing, the cell propagation capacity of HCT116 cells was decreased and the cell cycle progression was arrested. Ezrin expression was inhibited by the administration of baicalein in a dose-dependent way. The levels of CyclinD1 and CDK4 were also significantly decreased, but the expression of P53 pathway proteins P53 and P21 was markedly upregulated. Conclusion: Baicalein repressed proliferation of human colorectal cancer cells HCT116 and blocked cell cycle through downregulating Ezrin and upregulating P53 pathway-related proteins.

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Ezrin protein overexpression predicts the poor prognosis of pancreatic ductal adenocarcinomas

Cited by 38 publications

References 25 publications

Translational implication of Kallmann syndrome-1 gene expression in hepatocellular carcinoma

Translational implication of Kallmann syndrome-1 gene expression in hepatocellular carcinoma

Loss of ezrin in human intrahepatic cholangiocarcinoma is associated with ectopic expression of E‐cadherin

Baicalein Inhibits Proliferation Activity of Human Colorectal Cancer Cells HCT116 Through Downregulation of Ezrin

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