EGFR (Exon19del) A549 Cell Line

EGFR (Exon19del) A549 Cell Line is a human lung cancer cell line (A549) in which the native human epidermal growth factor receptor (EGFR) is not expressed due to CRISPR/Cas9 editing, and EGFR with an Exon19 deletion is 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 (Exon19del) Lentivirus (BPS Bioscience #82462). 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, being the most common mutation in GBM and breast cancer. 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. Deletion of Exon 19 is one of the most common EGFR oncogenic mutations, accounting for ~45% of EGFR mutations in NSCLC. Patients that respond to treatment with anti-EGFR therapy tend to develop resistance later on, highlighting the need for new therapeutic avenues.