EGFR A549 Cell Line

EGFR A549 Cell line is a human lung cancer cell line (A549) in which the endogenous human epidermal growth factor receptor (EGFR) is not expressed due to CRISPR/Cas9 editing, and where wildtype EGFR is now expressed under the control of an EF1a promoter. This cell line was generated by transduction of EGFR Knockout A549 cells (BPS Bioscience #83541) with EGFR Lentivirus (BPS Bioscience #82459). It was designed as a an appropriate control for EGFR mutant cell lines (BPS Bioscience #82478 and #82480). This cell line has been validated by flow cytometry. EGFR (epidermal growth factor receptor), also known as ERBB-1 and HER1, is the cell-surface tyrosine kinase receptor for members of the epidermal growth factor family. Its ligands include EGF, TGFalpha (transforming growth factor alpha), HB-EGF (heparin-binding EGF), betacellulin, amphiregulin, epiregulin and epigen. EGFR exists as an inactive monomer until it gets activated. Upon ligand binding it forms a homo- or heterodimer, for instance with HER2 (human epidermal growth factor receptor 2), which induces autophosphorylation, creating binding sites for adaptor proteins such as GRB2 (growth factor receptor-bound protein 2) and/or CBL (Casitas B-lineage lymphoma). EGFR can bind to several adaptor proteins simultaneously and thus activate multiple positive and negative signaling pathways. Overexpression and/or hyperactivation of EGFR kinase is associated with several human cancers such as lung, glioblastoma (GBM), and epithelial tumors of the neck and head. Mutations in EGFR can result in constantly activated EGFR, allowing tumor cell proliferation and development of resistance to drugs. Its role in cancer has led to the development of anticancer therapeutics targeting EGFR. There are several clinically approved inhibitors, such as Erlotinib and Gefitinib, for the treatment of NSCLC (non-small cell lung cancer) and pancreatic cancer. In addition, several monoclonal antibodies have also been approved, namely Cetuximab. Patients that respond to anti-EGFR therapy tend to develop resistance, highlighting the need for further studies and new therapeutic avenues.