The EIF3J Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the human EIF3J gene has been disrupted to generate a loss-of-function model. This product provides a heterogeneous pool of HeLa cells harboring diverse editing events at the EIF3J locus, enabling functional studies of EIF3J-dependent translation control without clonal selection. The polyclonal format mitigates clonal artifacts and retains population-level heterogeneity, making it suitable for pooled screening applications and robust biological replicate comparisons.
The host cell line, HeLa, is an immortalized cervical adenocarcinoma epithelial cell line originating from a human cervical carcinoma. HeLa cells contain integrated human papillomavirus 18 (HPV-18) sequences and express the viral oncoproteins E6 and E7, which inactivate the tumor suppressors p53 and Rb, respectively. This genetic background drives uncontrolled proliferation and renders HeLa cells a widely employed model for cancer biology, particularly for studying oncogenic signaling, cell cycle dysregulation, and translational reprogramming in solid tumors.
EIF3J encodes a non-core subunit of the eukaryotic translation initiation factor 3 (eIF3) complex, which orchestrates recruitment of the 40S ribosomal subunit to mRNA. EIF3J stabilizes the eIF3-40S interaction and facilitates mRNA scanning, thereby regulating global protein synthesis. Its activity is modulated by upstream regulators including mTORC1, MYC, and MAPK signaling, placing it downstream of growth factor and nutrient sensing pathways. EIF3J interacts directly with core eIF3 subunits (eIF3A, eIF3B, eIF3C, eIF3D, eIF3E, eIF3F, eIF3G, eIF3H, eIF3I, eIF3K, eIF3L, eIF3M) and auxiliary factors such as eIF1, eIF1A, and eIF5, integrating environmental cues to control translation of proliferation-associated mRNAs.
In the HeLa cancer model, EIF3J disruption is expected to impair cap-dependent translation initiation, selectively reducing synthesis of proteins that drive cell cycle progression and oncogenic growth. Given HeLa cells’ reliance on elevated translation rates for sustained proliferation, EIF3J knockout provides a tool to dissect how dysregulated mTOR-MAPK-eIF3 signaling contributes to cervical adenocarcinoma and other solid tumors. The model can reveal vulnerabilities in the translational machinery that are essential for tumor cell viability, thereby illuminating potential therapeutic nodes within the eIF3 complex.
This polyclonal knockout product supports a broad range of research applications, including mechanistic dissection of translation initiation, eIF3 complex assembly, and selective mRNA translation. It is compatible with assays such as polysome profiling to assess ribosome loading, puromycin incorporation to measure global protein synthesis, and RNA-seq for translatome analysis. Cell-based phenotypic assays??MTS/MTT proliferation, flow cytometric cell cycle analysis, and Annexin V apoptosis staining??enable functional readouts of EIF3J loss. The cells are also suitable for screening small-molecule translation inhibitors or validating EIF3J as a target in cervical and other solid tumor contexts. For comprehensive technical support, contact Ascent Research.
