RNAi-mediated blocking of ezrin reduces migration of ectopic endometrial cells in endometriosis

Jiang, Qiaoying; Xia, Jianmei; Ding, Haigang; Fei, Xiang-Wei; Lin, Jizhen; Wu, Renyi

doi:10.1093/molehr/gas019

Cited by 27 publications

(16 citation statements)

References 37 publications

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“…ERM proteins are required for the formation of focal adhesion complexes and stress fibers downstream of Rho-GTPase activation. Knocking down the expression of ERM proteins using anti-sense oligonucleotides or siRNA affects cell-cell and cell-matrix adhesion [15,17,18]. Notably, ezrin and radixin, the other members of the ERM family, showed no significant differential expression in GBM and normal brain tissues as revealed by our iTRAQ analysis.…”

Section: Discussionmentioning

confidence: 98%

“…Moesin belongs to the ERM (ezrin, radixin, moesin) family of proteins that functions as molecular cross-linkers between plasma membrane and cytoplasmic actin filaments [15,17,18]. ERM proteins are actively involved in actin cytoskeleton reorganization in response to several growth stimuli and serve as substrates for growth factor receptors including CD44, CD43, E-cadherin and intercellular adhesion molecule (ICAM-1, ICAM-2 and ICAM-3) [15].…”

Section: Discussionmentioning

confidence: 99%

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Role of moesin in hyaluronan induced cell migration in glioblastoma multiforme

et al. 2013

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BackgroundA major barrier to effective treatment of glioblastoma multiforme (GBM) is the invasion of glioma cells into the brain parenchyma rendering local therapies such as surgery and radiation therapy ineffective. GBM patients with such highly invasive and infiltrative tumors have poor prognosis with a median survival time of only about a year. However, the mechanisms leading to increased cell migration, invasion and diffused behavior of glioma cells are still poorly understood.MethodsIn the current study, we applied quantitative proteomics for the identification of differentially expressed proteins in GBMs as compared to non-malignant brain tissues.ResultsOur study led to the identification of 23 proteins showing overexpression in GBM; these include membrane proteins, moesin and CD44. The results were verified using Western blotting and immunohistochemistry in independent set of GBM and non-malignant brain tissues. Both GBM tissues and glioma cell lines (U87 / U373) demonstrated membranous expression of moesin and CD44, as revealed by immunohistochemistry and immunofluorescence, respectively. Notably, glioma cells transfected with moesin siRNA displayed reduced migration and invasion on treatment with hyaluronan (HA), an important component of the extracellular matrix in GBM. CD44, a transmembrane glycoprotein, acts as a major receptor for hyaluronan (HA). Using co-immunoprecipitation assays, we further demonstrated that moesin interacts with CD44 in glioma cells only after treatment with HA; this implicates a novel role of moesin in HA-CD44 signaling in gliomas.ConclusionsOur results suggest that development of inhibitors which interfere with CD44-moesin interactions may open a new avenue in the future to mitigate cellular migration in gliomas.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Role of moesin in hyaluronan induced cell migration in glioblastoma multiforme

et al. 2013

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“…However the present study is the first to show that chondrogenic differentiation increases ERM expression leading to increased membrane-cortex adhesion which in turn influences cell mechanics by reducing bleb formation. ERM expression is also linked to bleb-based motility 26 and thus the observed reduction in cell migration with differentiation may reflect the increased membrane-cortex adhesion and reduced bleb formation. We therefore suggest that stem cells are inherently blebby (high propensity to form blebs) due to low expression of ERM and that this influences characteristic stem cell behavior such as the ability to migrate.…”

Section: Discussionmentioning

confidence: 99%

Stem cell differentiation increases membrane-actin adhesion regulating cell blebability, migration and mechanics

Sliogeryte

Thorpe

Lee

et al. 2014

Sci Rep

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This study examines how differentiation of human mesenchymal stem cells regulates the interaction between the cell membrane and the actin cortex controlling cell behavior. Micropipette aspiration was used to measure the pressure required for membrane-cortex detachment which increased from 0.15 kPa in stem cells to 0.71 kPa following chondrogenic differentiation. This effect was associated with reduced susceptibility to mechanical and osmotic bleb formation, reduced migration and an increase in cell modulus. Theoretical modelling of bleb formation demonstrated that the increased stiffness of differentiated cells was due to the increased membrane-cortex adhesion. Differentiated cells exhibited greater F-actin density and slower actin remodelling. Differentiated cells also expressed greater levels of the membrane-cortex ezrin, radixin, moeisin (ERM) linker proteins which was responsible for the reduced blebability, as confirmed by transfection of stem cells with dominant active ezrin-T567D-GFP. This study demonstrates that stem cells have an inherently weak membrane-cortex adhesion which increases blebability thereby regulating cell migration and stiffness.

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“…The blockade of ezrin via RNA interference reduced the migration of ectopic endometrial cells and decreased the expression levels of RhoA and ROCK. These results suggest that the Ezrin/RhoA/ROCK pathway is a potential therapeutic target for the treatment of endometriosis (Jiang et al 2012). …”

Section: Ezrin Modulates Signal Transduction Pathwaysmentioning

confidence: 94%

Ezrin Orchestrates Signal Transduction in Airway Cells

Yin

Duan

Ulloa

et al. 2017

Reviews of Physiology, Biochemistry and Pharmacology

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Ezrin is a critical structural protein that organizes receptor complexes and orchestrates their signal transduction. In this study, we review the ezrin-meditated regulation of critical receptor complexes, including the epidermal growth factor receptor (EGFR), CD44, vascular cell adhesion molecule (VCAM), and the deleted in colorectal cancer (DCC) receptor. We also analyze the ezrin-meditated regulation of critical pathways associated with asthma, such as the RhoA, Rho-associated protein kinase (ROCK), and protein kinase A (cAMP/PKA) pathways. Mounting evidence suggests that ezrin plays a role in controlling airway cell function and potentially contributes to respiratory diseases. Ezrin can participate in asthma pathogenesis by affecting bronchial epithelium repair, T lymphocyte regulation, and the contraction of the airway smooth muscle cells. These studies provide new insights for the design of novel therapeutic strategies for asthma treatment.

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RNAi-mediated blocking of ezrin reduces migration of ectopic endometrial cells in endometriosis

Cited by 27 publications

References 37 publications

Role of moesin in hyaluronan induced cell migration in glioblastoma multiforme

Role of moesin in hyaluronan induced cell migration in glioblastoma multiforme

Stem cell differentiation increases membrane-actin adhesion regulating cell blebability, migration and mechanics

Ezrin Orchestrates Signal Transduction in Airway Cells

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