EOL-1 In Vitro Cellular Senescence Assay (Senescence)
CAT#: ITS-1122-YF3828
Target Cell Organism: Human
Target Cell Alternative Name: EoL-1
Target Cell Name: EOL-1
Assay Type: Cellular Senescence in Cancer Assays
Assay Overview
This assay is to provide EOL-1-based In Vitro Cellular Senescence Assay (Senescence) to accelerate our client's oncology projects. The assay will be customized according to the specific requirements. Please contact our scientists to discuss more details.
Target Cell Name
EOL-1
Target Cell Organism
Human
Target Cell Background
EoL-1 cells, a recently established human eosinophilic leukemia cell line, have cytological features of myeloblasts under normal culture conditions, and differentiate not only phenotypically but also functionally into eosinophils by a number of stimuli.
Target Cell Alternative Name
EoL-1
Related Diseases
Leukemia
Research Area
Oncology
Assay Name
In Vitro Cellular Senescence Assay (Senescence)
Short Description
EOL-1-cell based In Vitro Cellular Senescence Assay (Senescence)
Assay Description
Although numbers of various oncogenes and tumor suppressor genes have been proven to regulate senescence in normal cells, evading cellular senescence appears to be a significant step in cancer. Lysosomal senescence-associated β-galactosidase (SA-β-gal) is one of the common markers used to identify senescent cells. Senescence-associated secretory phenotype (SASP) secretion is a characteristic of senescent cells and several cytokines (interleukins 6 and 8), proteases (stromelysin-1), growth factors (vascular endothelial growth factor [VEGF]) and ECM components are some of the examples for SASPs. During early stages, SASP components help to promote migration of effector immune cells, tissue repair and release of proteases and growth factors. p53, pRb signaling (ALDH1A3, CCNA2 and AKT1) and some cell cycle genes (CDK4, CDK6 and CDK4) have been identified as genes controlling cellular senescence.
Assay Type
Cellular Senescence in Cancer Assays
Assay Type Details
Cell senescence is described as an irreversible physiological event of cell growth arrest, which is known to be caused by alterations of telomeres, oxidative stress, DNA damage and some oncogenes. Inhibition of the program of senescence is one of the main features of tumor cells and it has been reported that cancer cells can be induced to undergo senescence by chemo- and radiotherapies and genetic alterations. Telomeres help to prevent uncontrolled cell proliferation and the absence of telomeres results in aneuploidy and cell death.