The EIF3C Knockout HeLa Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, engineered to disrupt the EIF3C gene. This loss-of-function model enables systematic investigation of EIF3C function in translation initiation and oncogenic signaling. The polyclonal format provides a heterogeneous mixture of edited cells, reflecting the diversity of CRISPR-induced gene disruptions without single-cell cloning, and is suitable for pooled functional studies and high-throughput screening applications.
The parental HeLa cell line is a widely used human epithelial model isolated from a cervical adenocarcinoma and is positive for human papillomavirus type 18 (HPV18). These immortalized cells exhibit robust growth, are easy to transfect, and have been instrumental in cancer research, virology, and cell biology. The HeLa background is particularly relevant for studying EIF3C, as dysregulated translation is a hallmark of cervical carcinoma, and EIF3C overexpression has been linked to tumor progression in multiple cancer types, including cervical adenocarcinoma.
EIF3C encodes the c subunit of the eukaryotic translation initiation factor 3 (eIF3) complex, which is essential for cap-dependent mRNA recruitment to the ribosome. The eIF3 complex, comprising subunits such as eIF3A and eIF3B, interacts with eIF4G and RNA helicases to facilitate ribosomal scanning and initiation. EIF3C functions downstream of mTORC1, which integrates signals from insulin/IGF and EGF pathways to regulate translation via effectors like RAPTOR, S6K1, and 4E-BP1. Disruption of EIF3C impairs eIF3 complex integrity, resulting in reduced translation of key oncogenic mRNAs, including MYC, CCND1 (cyclin D1), and VEGF. This mechanistic connection places EIF3C at a critical node linking growth factor signaling to protein synthesis and tumorigenesis.
In HeLa cells, which harbor HPV18 oncogenes that manipulate host translation machinery, knockout of EIF3C provides a powerful system to dissect how viral and cellular factors converge on the translational apparatus. The EIF3C polyclonal knockout model enables researchers to study the consequences of impaired eIF3 function in a cancer-relevant context, including effects on cell proliferation, survival, and migratory capacity. This is particularly valuable for understanding the role of EIF3C in cervical adenocarcinoma and its potential as a therapeutic target, given that many cancers exhibit heightened translation initiation activity.
Typical applications encompass cancer biology and translational research, including functional genomics screens, drug resistance testing, and cervical cancer modeling. Researchers can employ these cells in a variety of assays, such as Western blotting and RT-qPCR to confirm EIF3C loss, polysome profiling and RNA-seq to assess global translatome changes, cap-binding assays to measure eIF4F complex activity, and cell-based proliferation, migration, and drug sensitivity assays. This product serves as a versatile platform for investigating translational control mechanisms and their impact on oncogenic signaling. For more information or to discuss technical specifications, please contact Ascent Research.
