The EGF Knockout HeLa Polyclonal Cells comprise a heterogeneous polyclonal population of HeLa cells harboring CRISPR/Cas9-mediated disruption of the EGF gene. This gene-edited product provides a loss-of-function model for investigating EGF-dependent signaling pathways in a human cervical adenocarcinoma background.
The parental HeLa cell line, derived from a human cervical adenocarcinoma, is an HPV18-positive epithelial model extensively employed in cancer biology, virology, and drug discovery. Its robust growth characteristics and well-characterized signaling networks make it a versatile platform for studying oncogenic processes.
EGF encodes a potent mitogen that, upon binding to its receptor EGFR, triggers receptor dimerization and autophosphorylation, initiating signal transduction through the GRB2-RAS-RAF1-MEK1/2-ERK1/2 cascade and the PI3K-AKT axis. This signaling network is modulated by upstream regulators such as TGF-??, STAT3, AP-1, HIF1A, and estradiol, while downstream effectors include ERK1/2, AKT, STAT3, FOS, JUN, and MYC. Additionally, the EGF-EGFR axis involves interaction with ADAM17, a sheddase that releases membrane-bound EGF precursors, providing a tightly controlled ligand-receptor system.
In the context of HPV18-driven cervical adenocarcinoma, EGF/EGFR signaling contributes to sustained cell proliferation, migration, and survival, partially overlapping with viral oncoprotein-mediated pathways. Ablation of EGF in HeLa cells enables dissection of autocrine and paracrine growth factor circuits, assessment of compensatory mechanisms, and evaluation of therapeutic vulnerabilities specific to cervical cancer.
Typical research applications include investigating ligand-receptor feedback, assessing pathway reactivation upon EGFR inhibitor treatment, and screening for novel therapeutic agents in cervical carcinoma. The polyclonal nature mirrors heterogeneous clinical samples, making these cells suitable for phospho-ERK1/2 detection after ligand stimulation, quantitative RT-qPCR of downstream targets such as FOS and JUN, and drug sensitivity profiling using MTT or migration assays. For further details and ordering information, please contact Ascent Research.
