Phenotypic heterogeneity in the NCI-H125 cell line affects biological activity using the epidermal growth factor receptor as target

• Published in: Acta pharmaceutica (Zagreb, Croatia) Vol. 62; no. 4; pp. 581 - 591
• Main Authors: Blanco, Rancés, Cedeño, Mercedes, González, Narjara, Rodríguez, Reynier, Sánchez, Javier, Rengifo, Enrique
• Format: Journal Article
• Language: English
• Published: Croatia 01.12.2012
• Subjects: Antibodies, Monoclonal, Humanized; Apoptosis - genetics; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - metabolism; Cell Cycle - genetics; Cell Division - genetics; Cell Line, Tumor; Cell Proliferation; Cell Survival - genetics; Flow Cytometry; Humans; Immunohistochemistry; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Phenotype; Receptor, Epidermal Growth Factor - genetics; Receptor, Epidermal Growth Factor - metabolism
• ISSN: 1846-9558
• DOI: 10.2478/v10007-012-0038-6

We evaluated the influence of some morphological changes of the NCI-H125 cell line in surface expression of the epidermal growth factor receptor (EGFR) and their impact on some biological activity assays using this molecule as target. Hematoxylin and eosin (H/E) staining, light microscopy immunocytochemistry, flow cytometric antibody-receptor binding test, cell viability determination and cell cycle analysis were performed. Phenotypic changes and inconsistency in EGFR expression were detected in NCI-H125 cell cultures. A significant reduction in the growth rate, mainly characterized by cell cycle arrest in the G0-G1 phase, was also evidenced. Differential distribution of cell viability in NCI-H125 subpopulations and its relationship with the EGFR surface expression were determined. Nuclear alterations observed in NCI- -H125 were not apoptosis related. A lack of control of cell cultures affects the reliability and reproducibility of biomedical and biotechnological research using EGFR as target. Therefore, rigorous control of the above mentioned parameters in these experiments is recommended.