scholarly journals Phenotypic heterogeneity in the NCI-H125 cell line affects biological activity using the epidermal growth factor receptor as target / Fenotipska heterogenost u staničnoj liniji NCI-H125 utječe na biološku aktivnost na receptore za epidermalni faktor rasta

2012 ◽  
Vol 62 (4) ◽  
pp. 581-591
Author(s):  
Rancés Blanco ◽  
Mercedes Cedeño ◽  
Narjara González ◽  
Reynier Rodríguez ◽  
Javier Sánchez ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Epidermal Growth Factor Receptor ◽  
Biological Activity ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Viability ◽  
Cell Cultures ◽  
Growth Factor Receptor ◽  
Surface Expression ◽  
Epidermal Growth

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.

scholarly journals LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way

2018 ◽  
Vol 45 (2) ◽  
pp. 523-536 ◽  
Author(s):  
Xiaohui Gong ◽  
Xianjin Du ◽  
Yong Xu ◽  
Wenze Zheng
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth

Background/Aims: LINC00037 has previously been reported to be up-regulated in clear cell renal cell carcinoma (ccRCC), however, the underlying mechanism remained unknown. In this study, we designed to investigate the functional role of LINC00037 in ccRCC Methods: LINC00037 knockdown and re-expressing 786-O and A498 cells were established. CCK8 assay and EdU assay were performed to evaluate the proliferation rates of ccRCC cells. Flow cytometry assay was performed to detect the cell apoptosis and cell cycle. Subcutaneous injection xenotransplantation mouse model was used to observe the role of LINC00037 in tumor growth in vivo. Mass spectrometry (MS) was performed to find the interacting partner of LINC00037 and RNA immunoprecipitation (RIP) was carried out to validate their interaction. Results: We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR. Conclusion: LINC00037 could inhibit proliferation of ccRCC in an epidermal growth factor receptor-dependent way.

Biological Activity In Vitro of Anti-Epidermal Growth Factor Receptor Monoclonal Antibodies with Different Affinities

Hybridoma ◽  
2007 ◽  
Vol 26 (6) ◽  
pp. 423-432 ◽  
Author(s):  
Arlhee Diaz Miqueli ◽  
Rances Blanco ◽  
Beatriz Garcia ◽  
Teresita Badia ◽  
Ana E. Batista ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Biological Activity ◽  
Monoclonal Antibodies ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth

scholarly journals Two chimeric receptors of epidermal growth factor receptor and c-Ros that differ in their transmembrane domains have opposite effects on cell growth.

1996 ◽  
Vol 16 (4) ◽  
pp. 1509-1518 ◽  
Author(s):  
Q Xiong ◽  
J L Chan ◽  
C S Zong ◽  
L H Wang
Keyword(s):  
Cell Cycle ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Cell Growth ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Signaling Proteins ◽  
Chimeric Receptors ◽  
Ideal System ◽  
Epidermal Growth

Two chimeric receptors, ER1 and ER2, were constructed. ER1 contains the extracellular and transmembrane (TM) domains derived from epidermal growth factor receptor and the cytoplasmic domain from c-Ros; ER2 is identical to ER1 except that its TM domain is derived from c-Ros. Both chimeras can be activated by epidermal growth factor and are capable of activating or phosphorylating an array of cellular signaling proteins. Both chimeras promote colony formation in soft agar with about equal efficiency. Surprisingly, ER1 inhibits while ER2 stimulates cell growth on monolayer culture. Cell cycle analysis revealed that all phases, in particular the S and G2/M phases, of the cell cycle in ER1 cells were elongated whereas G1 phase of ER2 cells was shortened threefold. Comparison of signaling pathways mediated by the two chimeras revealed several differences. Several early signaling proteins are activated or phosphorylated to a higher extent in ER1 than in ER2 cells in response to epidermal growth factor. ER1 is less efficiently internalized and remains tyrosine phosphorylated for a longer time than ER2. However, phosphorylation of the 66-kDa She protein, activation of mitogen activated protein kinase, and induction of c-fos and c-jun occur either to a lesser extent or for a shorter time in ER1 cells. Cellular protein phosphorylation patterns are also different in ER1 and ER2 cells. In particular, a 190-kDa Shc-associated protein is tyrosine phosphorylated in ER2 but not in ER1 cells. Our results indicate that the TM domains have a profound effect on the signal transduction and biological activity of those chimeric receptors. The results also imply that sustained stimulation of ER1 due to its retarded internalization apparently triggers an inhibitory response that dominantly counteracts the receptor-mediated mitogenic signals. These two chimeras, expressed at similar levels in the same cell type but having opposite effects on cell growth, provide an ideal system to study the mechanism by which a protein tyrosine kinase inhibits cell growth.

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