This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population in which the human IGF2BP3 gene has been disrupted via non-homologous end joining, generating a heterogeneous pool of HCT 116 cells with loss-of-function genotypes. As a polyclonal derivative, the population retains genetic diversity while collectively abrogating IGF2BP3 protein expression, providing a robust model for studying the gene’s role in colorectal carcinoma. The knockout model is derived from the HCT 116 cell line and is intended for advanced biomedical research applications, including functional genomics, signaling pathway dissection, and drug target validation.
The host cell line, HCT 116, is an epithelial cell line established from a human colorectal carcinoma. It harbors a KRAS G13D mutation and is deficient in MLH1, leading to microsatellite instability (MSI). These characteristics make HCT 116 a widely used model for investigating oncogenic KRAS-driven signaling, DNA mismatch repair deficiency, and colorectal cancer biology. The cell line is adherent and maintains key features of colorectal tumor cells, including dysregulated proliferation, apoptosis resistance, and metastatic potential, which are directly relevant to the functional outputs of IGF2BP3.
IGF2BP3 is an oncofetal RNA-binding protein that post-transcriptionally regulates a network of mRNAs. It stabilizes and enhances the translation of transcripts such as IGF2, MYC, and CD44, thereby promoting cell growth and invasive behavior. IGF2BP3 is transcriptionally activated by MYC and Wnt/??-catenin signaling and is negatively regulated by let-7 miRNA. It interacts with ELAVL1, eIF4E, and LIN28B to form ribonucleoprotein complexes that modulate mRNA fate. Downstream, IGF2BP3-controlled mRNAs encode components of the PI3K-AKT and MAPK/ERK pathways, including IGF2 (ligand for IGF1R), MYC, CCND1, and MMP9, establishing a feed-forward loop that sustains oncogenic signaling.
In the HCT 116 context, disruption of IGF2BP3 is expected to destabilize target mRNAs, attenuating the expression of IGF2, MYC, and CD44. This reduces signaling through the IGF1R?CPI3K?CAKT and RAS?CRAF?CMEK?CERK axes, impairing cell proliferation, migration, and invasion. Additionally, loss of IGF2BP3 may sensitize cells to apoptosis and enhance responsiveness to chemotherapeutic agents, given the cell line’s MSI status and reliance on these survival pathways. The model thus enables investigation of how IGF2BP3 sustains the malignant phenotype in an MSI colorectal cancer background.
This polyclonal knockout cell population is suitable for a range of experimental workflows. Researchers can employ it for functional rescue experiments, RNA immunoprecipitation to map IGF2BP3 mRNA targets, and phenotypic assays such as proliferation, migration, invasion, and apoptosis measurements. It supports drug sensitivity screening and synthetic lethality studies in the context of KRAS-mutant colorectal cancer. Transcriptomic analyses via RNA-seq and targeted expression profiling by RT-qPCR or western blotting can be performed to dissect pathway perturbations. For additional information, please contact Ascent Research.
