The IGF2BP3 Knockout SK-OV-3 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population for studying loss-of-function of the IGF2BP3 gene in the human SK-OV-3 ovarian adenocarcinoma cell line. This product consists of a mixed population of cells with targeted gene disruption, generated through CRISPR/Cas9-mediated genomic editing. The polyclonal format minimizes clonal artifacts and preserves genetic diversity, making it suitable for robust functional screens and comparative analyses.
SK-OV-3 is an adherent epithelial cell line derived from the ascitic fluid of a 64-year-old patient with ovarian serous cystadenocarcinoma. This cell line exhibits tumorigenicity in nude mice and serves as a well-established model for high-grade serous ovarian carcinoma. SK-OV-3 cells are p53 null due to a homozygous TP53 deletion and display expression of EGFR and HER2, recapitulating molecular features of advanced ovarian cancer.
IGF2BP3 is an oncofetal mRNA-binding protein that post-transcriptionally stabilizes oncogenic transcripts such as CD164, c-MYC, and MMP9, thereby enhancing their translation and driving cell proliferation, migration, and epithelial-mesenchymal transition (EMT). Transcriptionally activated by MYC and ??-catenin/TCF, and modulated by LIN28B, ZEB1, and microRNAs miR-873 and miR-129-5p, IGF2BP3 interacts with RNA-binding partners including HuR, DHX9, and YBX1. Downstream, it upregulates targets like CDK6, E2F factors, PROM1, and ABCG2. IGF2BP3 functions at the nexus of PI3K/AKT and MAPK/ERK pathways, where it amplifies mitogenic signals and promotes EMT through Snail/Slug-mediated induction of MMP9.
In ovarian cancer, elevated IGF2BP3 correlates with tumor aggressiveness and resistance to platinum-based therapies. The p53-null, EGFR/HER2-expressing SK-OV-3 model provides a pathologically relevant context to dissect IGF2BP3-dependent mechanisms. Loss of IGF2BP3 is expected to destabilize key pro-survival and pro-invasive transcripts, potentially restoring chemosensitivity and reducing metastatic potential. This knockout model thus enables systematic investigation of IGF2BP3’s contributions to oncogenic signaling and drug resistance in high-grade serous carcinoma.
This polyclonal knockout cell population supports diverse experimental workflows, including RNA immunoprecipitation to map IGF2BP3 target transcripts, RT-qPCR and Western blotting for downstream effector validation, and Transwell assays to quantify migration and invasion. Cell proliferation and apoptosis assays, combined with chemosensitivity testing for agents such as cisplatin and paclitaxel, facilitate dissection of therapeutic vulnerabilities. Flow cytometry for CD133 and ABCG2, and reporter assays for 3??-UTR regulation, further enable in-depth functional characterization. For additional inquiries, please contact Ascent Research.
