Collective cell migration plays an important role in wound healing, organogenesis, and the progression of metastatic disease. Analysis of collective migration typically involves laborious and time-consuming manual tracking of individual cells within cell clusters over several dozen or hundreds of frames. Herein, we develop a label-free, automated algorithm to identify and track individual epithelial cells within a free-moving cluster. We use this algorithm to analyze the effects of partial E-cadherin knockdown on collective migration of MCF-10A breast epithelial cells directed by an electric field. Our data show that E-cadherin knockdown in free-moving cell clusters diminishes electrotactic potential, with empty vector MCF-10A cells showing 16% higher directedness than cells with E-cadherin knockdown. Decreased electrotaxis is also observed in isolated cells at intermediate electric fields, suggesting an adhesion-independent role of E-cadherin in regulating electrotaxis. In additional support of an adhesion-independent role of E-cadherin, isolated cells with reduced E-cadherin expression reoriented within an applied electric field 60% more quickly than control. These results have implications for the role of E-cadherin expression in electrotaxis and demonstrate proof-of-concept of an automated algorithm that is broadly applicable to the analysis of collective migration in a wide range of physiological and pathophysiological contexts.
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http://dx.doi.org/10.1007/s12195-016-0471-6 | DOI Listing |
FEBS J
January 2025
Department of Molecular Medicine, Biochemistry Unit, University of Pavia, Italy.
The trimeric intracellular cation channel B (TRIC-B), encoded by TMEM38B, is a potassium (K) channel present in the endoplasmic reticulum membrane, where it counterbalances calcium (Ca) exit. Lack of TRIC-B activity causes a recessive form of the skeletal disease osteogenesis imperfecta (OI), namely OI type XIV, characterized by impaired intracellular Ca flux and defects in osteoblast (OB) differentiation and activity. Taking advantage of the OB-specific Tmem38b knockout mouse (Runx2Cre;Tmem38b; cKO), we investigated how the ion imbalance affects the osteogenetic process.
View Article and Find Full Text PDFBMC Oral Health
January 2025
Department of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Basic and Translational Medicine on Head & Neck Cancer, Key Laboratory of Cancer Prevention and Therapy, West Huan-Hu Rd, Ti Yuan Bei, Hexi District, Tianjin, 300060, P.R. China.
Background: Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer with alarmingly high morbidity. The cancer-associated fibroblasts (CAFs) play a pivotal role in tumor development, while their specific mechanisms in OSCC remains largely unclear. Our object is to explore a CAFs-related biomarker in OSCC.
View Article and Find Full Text PDFCell Mol Biol Lett
January 2025
Epithelial Plasticity and Metastasis Group, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Universidade da Coruña (UDC), Xubias de Arriba 84, 15006, A Coruña, Spain.
Hakai protein (CBLL1 gene) was identified as an E3 ubiquitin ligase of E-cadherin complex, inducing its ubiquitination and degradation, thus inducing epithelial-to-mesenchymal transition. Most of the knowledge about the protein was associated to its E3 ubiquitin ligase canonical role. However, important recent published research has highlighted the noncanonical role of Hakai, independent of its E3 ubiquitin ligase activity, underscoring its involvement in the N-methyladenosine (mA) writer complex and its impact on the methylation of RNA.
View Article and Find Full Text PDFJ Thorac Dis
December 2024
Key Laboratory of Interventional Pulmonology of Zhejiang Province, Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Background: It has been proposed that repeated exposure of bronchial epithelial cells to atmospheric particulate matter (PM) could disrupt airway epithelial integrity and lead to epithelial-to-mesenchymal transition (EMT) and ultimately airway remodeling. The molecular mechanisms underlying PM-related bronchial epithelial EMT have not yet been elucidated. The aim of this research is to clarify the molecular mechanism of EMT upon PM exposure.
View Article and Find Full Text PDFDifferentiation
January 2025
Molecular, Cellular and Developmental Biology Department (MCD), Centre de Biologie Integrative (CBI), University of Toulouse, CNRS, UPS, 31062, Toulouse, France. Electronic address:
Matrix Metalloproteinases (MMPs) are known for their role in matrix remodeling via their catalytic activities in the extracellular space. Interestingly, these enzymes can also play less expected roles in cell survival, polarity and motility via other substrates (e.g.
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