EZR (Ezrin)

Through virtual screening, we identified NSC305787 as a selective destabiliser of the R495W mutant complex by disrupting key Trp495-pre-C-terminal loop Ezrin interactions and causing steric hindrance to PIP2 recruitment. Our findings identified mutation-dependent changes in drug binding that can guide the development and repurposing of compounds for targeting PODXL-related cancers and improve patient outcomes in PODXL-altered malignancies.

© 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland

Overexpression of Ezrin also improved the rim formation in HeLa cells upon addition of a calcium ionophore. Thus, the ERM proteins appear to participate in a mechanism that links actin filaments to the nuclear envelope.

[This retracts the article DOI: 10.3892/ol.2016.5046.].

EZR links cytoskeletal remodeling to STAT3 signalling to drive metastatic competence and paclitaxel resistance, nominating EZR as a potential therapeutic vulnerability in treatment-refractory breast cancer.

TM promotes melanoma cell plasticity and VM through FAK- and ezrin-dependent pathways. These findings position TM as a key regulator of tumor progression and suggest that targeting TM may offer a novel therapeutic strategy to disrupt cancer cell plasticity and suppress melanoma growth.

Here, ERM proteins are identified as modulators of erastin-induced ferroptosis...Notably, other pro-oxidants similarly attenuate ferroptosis at appropriate concentrations. Together, these results establish ERM proteins as regulators of ferroptosis and reveal an underappreciated group of ferroptosis inhibitors that engage ROS-NRF2-mediated redox-adaptation.

Intriguingly, cancer cells escape glycation and its cytopathological effects by expressing relatively higher levels of glyoxalase 1 (GLO1); pharmacological GLO1 inhibition renders cancer cells vulnerable to MG. Thus, inhibition of stromal glycation holds promise for incorporation into personalized oncotherapy.

This mini review examines the contrasting roles of FAK in GBM and NF2-mutant meningiomas to underscore the importance of biological context in therapeutic decisions. We propose that NF2-mutant meningiomas represent a model for context-specific, synthetic lethal targeting, exemplifying a functional oncogenomics approach to precision oncology.

This review provides a comprehensive and uniquely alphabetized overview of Ezrin associations with a wide array of diseases, making it the first of its kind to catalog Ezrin biological relevance from A to Z. We examine its structural and biochemical characteristics, underscoring its potential as a diagnostic and prognostic biomarker, as well as an emerging therapeutic target. By addressing critical knowledge gaps, this review highlights Ezrin central role at the intersection of cancer biology, immunology, and neurotherapeutics.

The positively charged Lys-577, as well as the hydrophobic Ile-580 in the αD-helix, are pivotal for F-actin binding. Besides electrostatic interactions (Lys-577), Ile-580 appears to be crucial and might mediate the interaction with the hydrophobic cleft of G-actin.

Overexpression of VEGF, HIF-1α, Ezrin, and p53 was strongly associated with increased mortality risk in osteosarcoma. These findings may guide patient counselling, biomarker panel optimization, and the development of targeted therapies.