The EIF4G3 Knockout A2780 Polyclonal Cells product provides a heterogeneous CRISPR/Cas9-edited A2780 population with disrupted EIF4G3 alleles. This polyclonal knockout model is generated from the human ovarian carcinoma A2780 cell line and is intended for loss-of-function studies of the EIF4G3 scaffold protein. The polyclonal format ensures coverage of diverse mutations without clonal selection, making it a versatile tool for translation initiation research in ovarian cancer. Researchers can use these cells to examine how EIF4G3 ablation impacts cap-dependent translation and downstream signaling pathways.
The parental A2780 cell line is a well-characterized human ovarian endometrioid adenocarcinoma model. These epithelial cells are widely used to investigate drug resistance, particularly platinum resistance, and oncogenic signaling. A2780 cells display active mTOR signaling and growth factor responsiveness, making them suitable for analyzing translation control pathways. Their utility includes xenograft tumor studies and recapitulation of ovarian cancer biology. Disrupting EIF4G3 in this context allows examination of translational reprogramming in malignant phenotypes.
EIF4G3 encodes a scaffold protein in the eIF4F complex, bridging eIF4E at the 5? cap and PABP at the poly-A tail, while recruiting the 40S ribosomal subunit via eIF3. It also interacts with eIF4A to enhance helicase activity and with MNK1 to phosphorylate eIF4E. Upstream, mTORC1 regulates EIF4G3 activity by integrating signals from PI3K-Akt, growth factors like EGF and insulin, amino acids, and energy status. When activated, EIF4G3 drives translation of structured 5? UTR mRNAs, including MYC, cyclin D1, BCL2, and VEGF, thereby connecting nutrient and mitogenic signals to the protein synthesis machinery controlling cell proliferation and survival.
In A2780 ovarian cancer cells, EIF4G3 knockout disrupts translation of eIF4E-dependent oncogenic mRNAs, helping dissect mTOR-driven translational programs. Loss of EIF4G3 may selectively reduce synthesis of proteins promoting cell cycle progression and survival, potentially sensitizing cells to mTOR inhibitors. This polyclonal knockout pool avoids clonal artifacts, offering a model that reflects heterogeneous tumor populations for drug screening and adaptation studies.
Typical applications include mechanistic studies of cap-dependent translation, mTOR signaling analysis, and functional investigation of EIF4G3 in ovarian cancer. Assays such as polysome profiling, puromycin incorporation, western blotting, RT-qPCR, cap affinity chromatography, cell proliferation assays, and RNA-seq are supported. The cells facilitate screening of translation inhibitors, target validation for translation-directed therapies, and drug sensitivity testing with mTOR inhibitors. For additional details, please contact Ascent Research.
