The EIF3H Knockout SK-OV-3 Polyclonal Cells product provides a ready-to-use CRISPR/Cas9-edited polyclonal cell population derived from the human SK-OV-3 ovarian adenocarcinoma cell line. This loss-of-function model features targeted disruption of the EIF3H gene, which encodes a core subunit of the eukaryotic translation initiation factor 3 (eIF3) complex. The polyclonal pool comprises a heterogeneous mixture of cells harboring diverse Cas9-mediated editing events at the EIF3H locus, thereby avoiding clonal bias and offering a robust platform for functional studies. The cells are supplied as a growing culture and can be employed directly in downstream assays after thawing and expansion.
The SK-OV-3 host cell line was originally established from the ascites of a 64-year-old Caucasian female patient with ovarian adenocarcinoma. This epithelial cell line retains wild-type TP53, harbors amplified ERBB2, and is widely utilized as a model for ovarian cancer biology, drug response profiling, and oncogenic signaling studies. Its well-characterized genomic background makes it particularly suitable for examining the impact of EIF3H loss on translation control in a disease-relevant context.
EIF3H functions as an integral component of the eIF3 complex, which orchestrates cap-dependent translation initiation by promoting ribosomal scanning and start codon selection. This subunit is regulated by upstream mitogenic and nutrient-sensing pathways, including mTORC1, MYC, EGFR, IGF1R, PI3K, and AKT. In turn, EIF3H facilitates the selective translation of key oncogenic mRNAs such as Cyclin D1, c-MYC, and BCL-2. Within the translation machinery, EIF3H interacts directly with other eIF3 subunits (A, B, C, D, E, F, G, I, J, K, L, M), eIF4G, the 40S ribosomal subunit, eIF1, eIF1A, eIF5, and the cap-binding complex. Knockout of EIF3H disrupts assembly of the 43S preinitiation complex, leading to global attenuation of protein synthesis and a selective decrease in the expression of proliferation-driving and anti-apoptotic proteins.
In the context of SK-OV-3 ovarian cancer cells, loss of EIF3H is predicted to markedly impair cell proliferation, clonogenic survival, and tumorigenic potential by dampening the translation of critical oncogenic factors downstream of ERBB2 and mTORC1. This model thus enables dissection of the post-transcriptional mechanisms that support ovarian adenocarcinoma growth. Moreover, it serves as a valuable tool for evaluating therapeutic vulnerabilities, including sensitivity to mTOR inhibitors or drugs targeting the translation machinery. The interplay between EIF3H disruption and the amplified ERBB2 signaling network in this cell line can shed light on combinatorial treatment strategies.
The EIF3H Knockout SK-OV-3 Polyclonal Cells are well-suited for a broad range of research applications, including mechanistic studies of cap-dependent translation initiation, ribosome profiling, polysome fractionation, global proteomics, and functional genomic screens. Typical assays performed with this model encompass Western blotting for EIF3H and its downstream targets (e.g., Cyclin D1, c-MYC), RT-qPCR for knockout verification, colony formation assays, MTS proliferation assays, flow cytometric cell cycle analysis, Annexin V apoptosis detection, and Transwell migration/invasion assays. This polyclonal knockout resource empowers investigators to probe translational control in ovarian cancer and to perform drug sensitivity screens that may identify synthetic lethal interactions or resistance mechanisms. For further information or to inquire about custom services, please contact Ascent Research.
