The EIF3H Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-mediated polyclonal knockout cell population generated by disrupting the EIF3H gene in the SK-HEP-1 human hepatic adenocarcinoma cell line. This product offers a heterogeneous loss-of-function model that circumvents clonal selection, enabling studies of translation regulation in a physiologically relevant cancer cell context. The targeted gene encodes a critical subunit of the eIF3 translation initiation complex.
The parental SK-HEP-1 line was established from the ascitic fluid of a 52-year-old male patient with liver adenocarcinoma. These cells uniquely co-express epithelial and endothelial markers, making them a recognized model for investigating hepatocellular carcinoma, tumor angiogenesis, and metastatic mechanisms. Their endothelial-like characteristics support studies of vascular mimicry and cell adhesion in cancer.
EIF3H serves as an essential scaffold within the eIF3 complex, promoting 43S pre-initiation complex assembly and cap-dependent translation. Its transcription is directly activated by MYC and E2F factors in response to mTORC1 signaling, while its function is coordinated with RPTOR, EIF4E, and RPS6KB1. EIF3H physically interacts with other eIF3 subunits, eIF4G, and the 40S ribosomal subunit to recruit initiator tRNA. Disruption of EIF3H specifically reduces translation of oncogenic mRNAs including MYC, CCND1, and BCL2, thereby dampening PI3K-Akt and mTOR-driven cell proliferation and survival programs.
In the SK-HEP-1 background, EIF3H knockout is anticipated to impair global protein synthesis and suppress production of key oncoproteins, leading to diminished proliferation, colony-forming capacity, and motility. The dual epithelial-endothelial nature of these cells additionally permits dissection of how translation control influences angiogenic mimicry and metastatic potential, adding a unique dimension to functional genomics studies.
This polyclonal EIF3H knockout cell population is well-suited for polysome profiling to monitor translation efficiency, Western blot analysis of downstream targets, and RT-qPCR quantification of translationally regulated mRNAs. Puromycin incorporation assays provide a direct readout of global translation rates. Phenotypic assays including MTT/BrdU proliferation, colony formation, and transwell migration/invasion can delineate the impact on tumorigenic behavior. RNA-seq transcriptome profiling further enables comprehensive pathway interrogation. These tools make the model valuable for screening translation-targeted therapeutics and elucidating mTOR pathway crosstalk in liver cancer. For further details, please contact Ascent Research.
