Related Experiment Video
Updated: Jul 23, 2025

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
Published on: July 20, 2014
Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways
Claudia Tito1, Ilaria Genovese2, Flavia Giamogante3
1Section of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy.
Abstract:
The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, malignant progression and resistance to chemotherapeutic drugs. The present work elucidates a functional mechanism that links calcium homeostasis to EGFR signaling in cancer. Sorcin and EGFR expression are significantly correlated and associated with reduced overall survival in cancer patients. Mechanistically, Sorcin directly binds EGFR protein in a calcium-dependent fashion and regulates calcium (dys)homeostasis linked to EGF-dependent EGFR signaling. Moreover, Sorcin controls EGFR proteostasis and signaling and increases its phosphorylation, leading to increased EGF-dependent migration and invasion. Of note, silencing of Sorcin cooperates with EGFR inhibitors in the regulation of migration, highlighting calcium signaling pathway as an exploitable target to enhance the effectiveness of EGFR-targeting therapies.
More Related Videos
Related Concept Videos
Mitogens and the Cell Cycle
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Chemotaxis and Direction of Cell Migration
Cancer Cell Migration through Invadopodia
Small GTPases - Ras and Rho
Three regulatory proteins control their activity:

