• Bisphenol analogs
• Disease risk
• Ovary
• mRNA-seq

• Female
• Animals
• Mice
• Humans
• Benzhydryl Compounds/toxicity
• Ovarian Diseases
• RNA, Messenger

• Cancer
• Cytoskeletal remodeling
• Ezrin
• Metastasis
• Prognostic biomarker
• Therapeutic target

O‐GlcNAcylation of intracellular proteins (O‐GlcNAc) is a post‐translational modification that often competes with phosphorylation in diverse cellular signaling pathways. Recent studies on human malignant tumors have demonstrated that O‐GlcNAc is implicated in cellular features relevant to metastasis. Here, we report that lysophosphatidic acid (LPA)‐induced ovarian cancer cell (OVCAR‐3) migration is regulated by O‐GlcNAc. We found that O‐GlcNAc modification of ERM family proteins, a membrane‐cytoskeletal crosslinker, was inversely correlated with its phosphorylation status. Moreover, the LPA‐induced formation of membrane protrusion structures, as well as the migration of OVCAR‐3 cells, was reduced by the accumulation of O‐GlcNAc. Collectively, these findings suggest that O‐GlcNAc is an essential signaling element controlling ERM family proteins involved in OVCAR‐3 cell migration.

• G protein
• actin
• cancer
• ciliogenesis
• cytoskeleton
• ezrin
• metastasis

• Actin Cytoskeleton/metabolism
• Actins/metabolism
• Cell Membrane/metabolism
• Cytoskeletal Proteins
• Microfilament Proteins/metabolism
• Phosphoproteins/metabolism

Ezrin, ERK, STAT3, and AKT are proteins that are overexpressed in various types of cancer, although their expressions in tongue cancer has received less focus. This study aimed to address associations between the expression levels of these proteins and with characteristics of the tumor and patient survival.

We performed immunohistochemical staining of ezrin, ERK, STAT3, and AKT in tumors from patients with tongue carcinoma in situ (CIS, n = 17) and tongue squamous cell carcinoma (SCC, n = 46). Statistical differences between the SCC versus the CIS cohorts were estimated by calculations of bivariate odds ratios of low versus high expression of the proteins. Fisher's exact tests were used to appraise interassociations between the proteins, as well as expression levels versus patient and tumor characteristics. Survival based on Kaplan–Meier statistics in combination log‐rank tests were used to address potential effects of the patient and tumor characteristics versus 5‐year survival rate.

The relative high: low expression of all four proteins in the two cohorts differed, and particularly ERK was markedly overexpressed in the SCC versus the CIS cohort (odds ratio = 45.3, p < .01). The relative high: low expression each protein versus patient and tumor characteristics; showed associations between AKT expression and T stage (p = .002) plus node metastases (p = .12), and between ERK expression and drinking (p = .01) and smoking history (p = .01). There was no significant difference observed between ERK and the three other molecules, nor any significant difference between the degree of expression of each protein and the 5‐year disease‐specific survival rate.

Ezrin, ERK, STAT3, and AKT appear to be involved in the progress from carcinoma in situ in the tongue into squamous cell carcinoma. ERK in particular is overexpressed, suggesting that ERK may be a novel therapeutic target for preventing tongue cancer.

• AKT
• ERK
• the 5-year survival rate
• tongue squamous cell carcinoma

Diabetic women have a 2–3 fold increased risk of developing endometrial cancer, however, the molecular aspects of this risk are not fully understood. This study investigated the alteration of cellular O-GlcNAcylation of proteins as the potential mechanistic connection between these two conditions. The endometrial cancer cell line (Ishikawa) was utilized to study the effect of dysregulation of O-GlcNAcylation on epithelial mesenchymal transition (EMT). Hyper-O-GlcNAcylation (via 1 μM Thiamet-G/ThmG or 25 mM Glucose) enhanced the expression of EMT-associated genes (WNT5B and FOXC2), and protein expression of the EMT adhesion molecule, N-Cadherin. Reorganization of stress filaments (actin filaments), consistent with EMT, was also noted in ThmG-treated cells. Interestingly, Hypo-O-GlcNAcylation (via 50 μM OSMI-1) also upregulated WNT5B, inferring that any disruption to O-GlcNAc cycling impacts EMT. However, Hypo-O-GlcNAcylation reduced overall cellular proliferation/migration and the expression of pro-EMT genes (AHNAK, TGFB2, FGFBP1, CALD1, TFPI2). In summary, disruption of O-GlcNAc cycling (i.e., Hyper- or Hypo-O-GlcNAcylation) promoted EMT at both the molecular and cellular levels, but only Hyper-O-GlcNAcylation provoked cellular proliferation/migration, and cytoskeletal reorganization.

• O-GlcNAc
• diabetes
• endometrial cancer
• epithelial-mesenchymal transition
• metastasis

• Animals
• Bone and Bones/cytology
• Cell Proliferation/drug effects
• Cells, Cultured
• Coated Materials, Biocompatible/chemistry
• Coated Materials, Biocompatible/pharmacology
• Copper/chemistry
• Electrochemical Techniques
• Escherichia coli/drug effects
• Magnesium/chemistry
• Materials Testing
• Mice
• Oxidation-Reduction
• Phytic Acid/chemistry
• Rabbits
• Random Allocation
• Staphylococcus aureus/drug effects
• Ultrasonics

Mesenchymal stem cells (MSC) display tumor tropism and have been addressed as vehicles for delivery of anti-cancer agents. As cellular components of the tumor microenvironment, MSC also influence tumor progression. However, the contribution of MSC in brain cancer is not well understood since either oncogenic or tumor suppressor effects have been reported for these cells. Here, MSC were found capable of stimulating human Glioblastoma (GBM) cell proliferation through a paracrine effect mediated by TGFB1. Moreover, when in direct cell-cell contact with GBM cells, MSC elicited an increased proliferative and invasive tumor cell behavior under 3D conditions, as well as accelerated tumor development in nude mice, independently of paracrine TGFB1. A secretome profiling of MSC-GBM co-cultures identified 126 differentially expressed proteins and 10 proteins exclusively detected under direct cell-cell contact conditions. Most of these proteins are exosome cargos and are involved in cell motility and tissue development. These results indicate a dynamic interaction between MSC and GBM cells, favoring aggressive tumor cell traits through alternative and independent mechanisms. Overall, these findings indicate that MSC may exert pro-tumorigenic effects when in close contact with tumor cells, which must be carefully considered when employing MSC in targeted cell therapy protocols against cancer.

• aggressiveness
• glioblastoma
• mesenchymal stem cells
• secretome
• tumor microenvironment

Colorectal cancer (CRC)-associated mortality is primarily caused by lymph node (LN) and distant metastasis, highlighting the need for biomarkers that predict LN metastasis and facilitate better therapeutic strategies. We used an Isobaric Tags for Relative and Absolute Quantification (iTRAQ)-based comparative proteomics approach to identify novel biomarkers for predicting LN metastasis in CRC patients. We analyzed five paired samples of CRC with or without LN metastasis, adjacent normal mucosa, and normal colon mucosa, and differentially expressed proteins were identified and subsequently validated at the protein and/or mRNA levels by immunohistochemistry and qRT-PCR, respectively. We identified 55 proteins specifically associated with LN metastasis, from which we selected ezrin for further analysis and functional assessment. Expression of ezrin at both the protein and mRNA levels was significantly higher in CRC tissues than in adjacent normal colonic mucosa. In univariate analysis, high ezrin expression was significantly associated with tumor progression and poor prognosis, which was consistent with our in vitro findings that ezrin promotes the metastatic capacity of CRC cells by enabling cell invasion and migration. In multivariate analysis, high levels of ezrin protein and mRNA in CRC samples were independent predictors of LN metastasis. Our data thus identify ezrin as a novel protein and mRNA biomarker for predicting LN metastasis in CRC patients.

• biomarker
• colorectal cancer
• ezrin
• iTRAQ-based quantitative proteomic analysis
• lymph node metastasis

• carcinogenesis
• cervical cancer
• estradiol
• ezrin

Ezrin and p130Cas are structural proteins with an important role in signaling pathways and have been shown to promote cancer dissemination. We previously reported on overexpression of both ezrin and p130Cas in breast carcinoma effusions compared to primary carcinomas. Since ovarian and breast carcinomas share the ability to disseminate by forming malignant effusions, we sought to study the role of these molecules in ovarian carcinoma (OC).

OC cell lines were cultured in two different 3-dimensional conditions, on alginate scaffolds and as spheroids, which served as models for solid tumor and malignant effusions, respectively. shRNA was used to reduce protein expression in the cells. The malignant potential was evaluated by chemo-invasion assay, branching capacity on Matrigel and rate of proliferation. Subsequently, clinical specimens of high-grade serous carcinoma effusions, ovarian tumors and solid metastases were analyzed for ezrin and p130Cas expression.

Higher ezrin expression was found in cells composing the spheroids compared to their counterparts cultured on alginate scaffold and in clinical samples of malignant effusions compared to solid tumors. In addition, reduced Ezrin expression impaired the invasion ability and the branching capacity of OC cells to a greater extent than reduced p130Cas expression. However, ezrin and p130Cas expression in effusions was unrelated to clinical outcome.

The 3-dimensional cell cultures were found to mimic the different tumor sites and be applicable as a model. The in vitro results concur with the clinical specimen analysis, suggesting that in OC, the role of ezrin in disease progression is more pronounced than that of p130Cas.

High recurrence rate is one representative characteristic of bladder cancer. Intravesical therapy after transurethral resection is often performed in patients with nonmuscle invasive bladder cancer (NMIBC) to prevent recurrence. Bacillus Calmette-Guérin (BCG) and several anticancer/antibiotic agents, such as mitomycin C and epirubicin, are commonly used for this therapy. BCG treatment demonstrates strong anticancer effects. However, it is also characterized by a high frequency of adverse events. On the other hand, although intravesical therapies using other anticancer and antibiotic agents are relatively safe, their anticancer effects are lower than those obtained using BCG. Thus, the appropriate selection of agents for intravesical therapy is important to improve treatment outcomes and maintain the quality of life of patients with NMIBC. In this review, we discuss the predictive value of various histological and molecular markers for recurrence after intravesical therapy in patients with NMIBC.

• Androgen receptor
• angiotensin II
• endometrial cancer

• Angiotensin II/genetics
• Angiotensin II/metabolism
• Endometrial Neoplasms/genetics
• Endometrial Neoplasms/metabolism
• Female
• Humans
• Receptors, Androgen/genetics
• Receptors, Androgen/metabolism
• Receptors, Angiotensin/genetics
• Receptors, Angiotensin/metabolism
• Up-Regulation
• Vascular Endothelial Growth Factor A/genetics
• Vascular Endothelial Growth Factor A/metabolism

Reduced membranous expression of the cytoskeleton-associated protein ezrin has previously been demonstrated to correlate with tumour progression and poor prognosis in patients with T1G3 urothelial cell carcinoma of the bladder treated with non-maintenance Bacillus Calmette-Guérin (n = 92), and the associations with adverse clinicopathological factors have been validated in another, unselected, cohort (n = 104). In the present study, we examined the prognostic significance of ezrin expression in urothelial bladder cancer in a total number of 442 tumours from two independent patient cohorts.

Immunohistochemical expression of ezrin was evaluated in tissue microarrays with tumours from one retrospective cohort of bladder cancer (n = 110; cohort I) and one population-based cohort (n = 342; cohort II). Classification regression tree analysis was applied for selection of prognostic cutoff. Kaplan-Meier analysis, log rank test and Cox regression proportional hazards’ modeling were used to evaluate the impact of ezrin on 5-year overall survival (OS), disease-specific survival (DSS) and progression-free survival (PFS).

Ezrin expression could be evaluated in tumours from 100 and 342 cases, respectively. In both cohorts, reduced membranous ezrin expression was significantly associated with more advanced T-stage (p < 0.001), high grade tumours (p < 0.001), female sex (p = 0.040 and p = 0.013), and membranous expression of podocalyxin-like protein (p < 0.001 and p = 0.009). Moreover, reduced ezrin expression was associated with a significantly reduced 5-year OS in both cohorts (HR = 3.09 95% CI 1.71-5.58 and HR = 2.15(1.51-3.06), and with DSS in cohort II (HR = 2.77, 95% CI 1.78-4.31). This association also remained significant in adjusted analysis in Cohort I (HR1.99, 95% CI 1.05-3.77) but not in Cohort II. In pTa and pT1 tumours in cohort II, there was no significant association between ezrin expression and time to progression.

The results from this study validate previous findings of reduced membranous ezrin expression in urothelial bladder cancer being associated with unfavourable clinicopathological characteristics and an impaired survival. The utility of ezrin as a prognostic biomarker in transurethral resection specimens merits further investigation.

Ezrin, a member of the ezrin/radixin/moesin (ERM) protein family, plays a pivotal role in tumor invasion and metastasis. This study is aimed to investigate the clinicopathological significance of upregulated ezrin protein expression in uterine cervical cancers.

Immunohistochemical staining of ezrin protein was performed on uterine cervical cancer specimens from 235 patients. For comparison, 239 cases of cervical intraepithelial neoplasia (CIN), 17 cases of cervical glandular intraepithelial neoplasia (CGIN) and 52 normal cervix samples were also included. qRT-PCR was performed on fresh tissues to detect ezrin mRNA expression levels. HPV infection statuses were genotyped by oligonucleotide microarray, and 10-year survival rates were calculated using the Kaplan-Meier method for 109 cervical cancer patients.

Apical membranous distribution of ezrin protein was only observed in normal cervical glands, while perinuclear staining was only observed in cervical cancers. Strong cytoplasmic and diffuse localization of ezrin were frequently seen in the cervical cancers compared with the normal counterparts. Furthermore, this strongly positive ezrin expression was significantly higher in cervical cancers than in CIN, CGIN, and normal cervical epithelia. Ezrin overexpression was closely related with poor differentiation, late stage, and lymph node metastasis. Additionally, ezrin overexpression was associated with lower 10-year survival rate for patients with early stage cervical cancer, but not for patients with advanced stage.

Aberrant localization and overexpression of ezrin might be an independent effective biomarker for prognostic evaluation of cervical cancers.

Endometrial cancer is the most common gynecologic malignancy in the United States but it remains poorly understood at the molecular level. This investigation was conducted to specifically assess whether gene expression changes underlie the clinical and pathologic factors traditionally used for determining treatment regimens in women with stage I endometrial cancer. These include the effect of tumor grade, depth of myometrial invasion and histotype. We utilized oligonucleotide microarrays to assess the transcript expression profile in epithelial glandular cells laser microdissected from 79 endometrioid and 12 serous stage I endometrial cancers with a heterogeneous distribution of grade and depth of myometrial invasion, along with 12 normal post-menopausal endometrial samples. Unsupervised multidimensional scaling analyses revealed that serous and endometrioid stage I cancers have similar transcript expression patterns when compared to normal controls where 900 transcripts were identified to be differentially expressed by at least fourfold (univariate t-test, p < 0.001) between the cancers and normal endometrium. This analysis also identified transcript expression differences between serous and endometrioid cancers and tumor grade, but no apparent differences were identified as a function of depth of myometrial invasion. Four genes were validated by quantitative PCR on an independent set of cancer and normal endometrium samples. These findings indicate that unique gene expression profiles are associated with histologic type and grade, but not myometrial invasion among early stage endometrial cancers. These data provide a comprehensive perspective on the molecular alterations associated with stage I endometrial cancer, particularly those subtypes that have the worst prognosis.

• DLG7
• IHH
• MELK
• RORB
• endometrial cancer
• gene expression
• stage I

Protein 4.1N belongs to the protein 4.1 superfamily that links transmembrane proteins to the actin cytoskeleton. Recent evidence has shown that protein 4.1 is important in tumor suppression. However, the functions of 4.1N in the metastasis of breast cancer are largely unknown. In the present study, MCF-7, T-47D and MDA-MB-231 breast cancer cell lines with various metastatic abilities were employed. Protein 4.1N was found to be expressed in poorly metastatic MCF-7 and middle metastatic T-47D cell lines, and was predominantly associated with cell-cell junctions. However, no 4.1N expression was detected in the highly metastatic MDA-MB-231 cells. Moreover, re-expression of 4.1N in MDA-MB-231 cells inhibited cell adhesion, migration and invasion. The results suggest that protein 4.1N is a negative regulator of cell metastasis in breast cancer.

Metastasis is the main cause of death in cancer and is a multistep process. Moesin (MSN), a member of the ezrin-rdixin-moesin family and Claudin7 (CLDN7), a tight junction protein, both play a role in tumor cell metastasis. Previously, we found an over-expression of MSN and under-expression of CLDN7 at the mRNA level in uterine serous carcinoma in comparison to uterine endometrioid adenocarcinoma. The purpose of this study is to determine the protein expression of MSN and CLDN7 in endometrial cancer (EC) and to evaluate their prognostic value. Two hundred sixty-five patients with EC were retrieved from the archives. MSN and CLDN7 immunostaining were performed on the tissue paraffin sections. The expression of each antibody was reported and then correlated with clinicopathological prognostic factors including age, tumor grade, tumor stage, lympho-vascular involvement, depth of myometrial invasion, overall survival (OS), disease free survival (DFS) and death of disease (DOD).

MSN and CLDN were expressed in 46% and 52% of overall cases. We observed an association between MSN⁺ staining and tumor grade, and serous and clear cell carcinoma subtypes (p < 0.001 each). There was an association between CLDN7⁺ staining and low tumor grade and endometrioid adenocarcinoma subtype (p < 0.001 and 0.001 respectively). However, no association between MSN and CLDN7 expression and outcome including OS, DOD, and DFS was found.

A significant prognostic value of MSN and CLDN7 in predicting disease outcomes in patients with EC was not demonstrated. Nevertheless, the high percentage of EC cases with MSN and CLDN7 immunoexpression, and their association with tumor grade and subtypes, suggests that these proteins might play a role in tumorigenesis of endometrial adenocarcinomas. Future studies are needed to shed light on their mechanistic properties in EC cells.

• Adenocarcinoma/genetics
• Adenocarcinoma/metabolism
• Adenocarcinoma/pathology
• Biomarkers, Tumor/biosynthesis
• Biomarkers, Tumor/genetics
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/pathology
• Cytoskeletal Proteins/biosynthesis
• Cytoskeletal Proteins/genetics
• Female
• Humans
• Lymphatic Metastasis
• Male
• Middle Aged
• Neoplasm Invasiveness
• Neoplasm Staging/methods
• Prognosis
• Survival

Endometrial cancer is the most common gynecologic malignancy in the developed countries. Clinical studies have shown that early stage uterine serous carcinoma (USC) has outcomes similar to early stage high grade endometrioid adenocarcinoma (EAC-G3) than to early stage low grade endometrioid adenocarcinoma (EAC-G1). However, little is known about the origin of these different clinical outcomes. This study applied the whole genome expression profiling to explore the expression difference of stage I USC (n = 11) relative to stage I EAC-G3 (n = 11) and stage I EAC-G1 (n = 11), respectively.

We found that the expression difference between USC and EAC-G3, as measured by the number of differentially expressed genes (DEGs), is consistently less than that found between USC and EAC-G1. Pathway enrichment analyses suggested that DEGs specific to USC vs. EAC-G3 are enriched for genes involved in signaling transduction, while DEGs specific to USC vs. EAC-G1 are enriched for genes involved in cell cycle. Gene expression differences for selected DEGs are confirmed by quantitative RT-PCR with a high validation rate.

This data, although preliminary, indicates that stage I USC is genetically similar to stage I EAC-G3 compared to stage I EAC-G1. DEGs identified from this study might provide an insight in to the potential mechanisms that influence the clinical outcome differences between endometrial cancer subtypes. They might also have potential prognostic and therapeutic impacts on patients diagnosed with uterine cancer.

• actin
• cofilin
• ezrin
• colon adenocarcinoma.

• Adenocarcinoma/metabolism
• Adenocarcinoma/pathology
• Cell Adhesion
• Cell Movement
• Cofilin 1/analysis
• Cofilin 1/metabolism
• Colonic Neoplasms/metabolism
• Colonic Neoplasms/pathology
• Cytoskeletal Proteins/analysis
• Cytoskeletal Proteins/metabolism
• Humans
• Immunohistochemistry
• Neoplasm Metastasis
• Tumor Cells, Cultured

• Carcinoma, Squamous Cell/etiology
• Carcinoma, Squamous Cell/genetics
• Cell Line, Tumor
• Chromosomal Instability
• Cytoskeletal Proteins/analysis
• Cytoskeletal Proteins/physiology
• Duodenogastric Reflux/complications
• Esophageal Neoplasms/etiology
• Esophageal Neoplasms/genetics
• Humans
• Immunohistochemistry

• Aged
• Biomarkers, Tumor/metabolism
• Blotting, Western
• Cell Line, Tumor
• Cell Proliferation
• Colon/metabolism
• Cytoskeletal Proteins/metabolism
• DNA Mutational Analysis
• Disease-Free Survival
• Female
• Gastrointestinal Stromal Tumors/genetics
• Gastrointestinal Stromal Tumors/metabolism
• Gastrointestinal Stromal Tumors/mortality
• Gastrointestinal Stromal Tumors/pathology
• Gastrointestinal Stromal Tumors/surgery
• Gene Expression Regulation, Neoplastic
• Humans
• Immunohistochemistry
• Kaplan-Meier Estimate
• Male
• Middle Aged
• Muscle, Smooth/metabolism
• Mutation
• Phosphorylation
• Proportional Hazards Models
• Proto-Oncogene Proteins c-kit/genetics
• Receptor, Platelet-Derived Growth Factor alpha/genetics
• Retrospective Studies
• Risk Assessment
• Threonine
• Time Factors
• Tissue Array Analysis
• Treatment Outcome
• Up-Regulation

Cell motility is controlled by the dynamic cytoskeleton and its related proteins, such as members of the ezrin/radixin/moesin (ERM) family, which act as signalling molecules inducing cytoskeleton remodelling. Although ERM proteins have been identified as important factors in various malignancies, functional redundancy between these proteins has hindered the dissection of their individual contribution. The aim of the present study was to analyse the functional role of moesin in pancreatic malignancies. Cancer cells of different malignant lesions of human and transgenic mice pancreata were evaluated by immunohistochemistry. For functional analysis, cell growth, adhesion and invasion assays were carried out after transient and stable knock-down of moesin expression in pancreatic cancer cells. In vivo tumourigenicity was determined using orthotopic and metastatic mouse tumour models. We now show that moesin knock-down increases migration, invasion and metastasis and influences extracellular matrix organization of pancreatic cancer. Moesin-regulated migratory activities of pancreatic cancer cells were in part promoted through cellular translocation of β-catenin, and re-distribution and organization of the cytoskeleton. Analysis of human and different transgenic mouse pancreatic cancers demonstrated that moesin is a phenotypic marker for anaplastic carcinoma, suggesting that this ERM protein plays a specific role in pancreatic carcinogenesis.

• ezrin
• erm
• pkc
• tumor metastasis

• Actins/metabolism
• Animals
• Bone Neoplasms/metabolism
• Bone Neoplasms/pathology
• Cell Line, Tumor
• Cell Movement
• Cytoskeletal Proteins/metabolism
• Cytoskeleton/metabolism
• Gene Expression Regulation, Neoplastic
• Humans
• Mice
• Neoplasm Metastasis
• Osteosarcoma/metabolism
• Osteosarcoma/pathology
• Protein Kinase C/metabolism
• Wound Healing

• Z01 BC010566 Intramural NIH HHS

• Adenocarcinoma/metabolism
• Adenocarcinoma/mortality
• Adult
• Aged
• Biomarkers, Tumor/metabolism
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/mortality
• Cytoplasm/metabolism
• Cytoskeletal Proteins/metabolism
• Female
• Fluorescent Antibody Technique, Direct
• Humans
• Immunoenzyme Techniques
• Kaplan-Meier Estimate
• Lymph Nodes/pathology
• Male
• Middle Aged
• Neoplasm Staging
• Predictive Value of Tests
• Prognosis
• Survival Rate
• Young Adult

AIM: To investigate the correlation between ezrin expression and types of gastric carcinoma and clinico-pathological variables.

METHODS: We examined ezrin protein expression in 75 gastric carcinoma (53 intestinal types of adenocarcinoma, 22 diffuse types of carcinoma) tissues by immunohistochemistry. The results were compared with clinicopathological parameters such as tumor type, grade of tumor, clinical stage, presence of metastatic lymph node, and depth of invasion.

RESULTS: Ezrin immunostaining was positive in 43 cases (81.1%) of intestinal type and in 9 (40.9%) cases of diffuse type adenocarcinomas (P < 0.001). In gastric carcinomas, the expression of ezrin protein correlated with the status of H pylori and survival. There was no correlation between expression of ezrin with TNM stage and histological grade of gastric carcinomas (P > 0.05).

CONCLUSION: The low expression of ezrin implicates the loss of adhesion in diffuse carcinomas. Furthermore, overexpression of ezrin in carcinomas with H pylori infection may be a genuine specific pathway in which H pylori may cause/initiate gastric carcinoma.

• Ezrin
• Gastric carcinoma
• H pylori
• Metastasis

• Adenocarcinoma/chemistry
• Adenocarcinoma/microbiology
• Adenocarcinoma/mortality
• Adenocarcinoma/pathology
• Cell Differentiation
• Cytoskeletal Proteins/analysis
• Helicobacter pylori/isolation & purification
• Humans
• Immunohistochemistry
• Neoplasm Invasiveness
• Neoplasm Staging
• Stomach Neoplasms/chemistry
• Stomach Neoplasms/microbiology
• Stomach Neoplasms/mortality
• Stomach Neoplasms/pathology

• Cell Adhesion Molecules/physiology
• Endometrial Neoplasms/etiology
• Endometrial Neoplasms/genetics
• Endometrial Neoplasms/pathology
• Female
• Gene Expression
• Humans
• Neoplasm Invasiveness

• Adolescent
• Adult
• Aged
• Biomarkers, Tumor/metabolism
• Child
• Cytoskeletal Proteins/metabolism
• Epidermal Growth Factor/metabolism
• Female
• Hepatocyte Growth Factor/metabolism
• Humans
• Immunoenzyme Techniques
• Liver Neoplasms/metabolism
• Liver Neoplasms/mortality
• Liver Neoplasms/secondary
• Lymphocytes, Tumor-Infiltrating/pathology
• Male
• Melanoma/metabolism
• Melanoma/mortality
• Melanoma/secondary
• Middle Aged
• Proto-Oncogene Proteins c-met/metabolism
• Survival Rate
• Uveal Neoplasms/metabolism
• Uveal Neoplasms/mortality
• Uveal Neoplasms/pathology

• Carcinoma/metabolism
• Carcinoma/pathology
• Cell Line, Tumor
• Cytoskeletal Proteins/metabolism
• Down-Regulation
• Gene Expression Regulation, Neoplastic/genetics
• Gene Expression Regulation, Neoplastic/physiology
• Humans
• Immunohistochemistry
• Membrane Proteins/genetics
• Membrane Proteins/metabolism
• Nasopharyngeal Neoplasms/metabolism
• Nasopharyngeal Neoplasms/pathology
• RNA Interference
• Transfection
• Tumor Suppressor Proteins/genetics
• Tumor Suppressor Proteins/metabolism

• Actins/metabolism
• Apoptosis
• Blotting, Western
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Cell Division
• Cell Membrane/metabolism
• Cell Proliferation
• Cytoskeletal Proteins/metabolism
• Cytoskeleton/metabolism
• Fluorescent Antibody Technique
• G2 Phase
• Humans
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• Neoplasm Invasiveness
• Pseudopodia
• RNA, Small Interfering/pharmacology
• Reverse Transcriptase Polymerase Chain Reaction
• Tumor Cells, Cultured